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Pesticide Detoxification

Genetically engineering ways to detoxify some of the poisonous pesticide residues. This essay highlights two such programs, the first probably a boon and the second more likely a potential boondoggle. The organochlorine and organophosphate pesticides that accumulate in soils and waters and concentrate in food webs consist of durable, ringlike organic molecules that break down only slowly. Ironically, some insects know how to accelerate the disintegration process. In the last few decades, in response to widespread chemical applications, these resilient insects have evolved enzyme systems that detoxify the poisons by cleaving their ring structures. Scientists in Australia now are hoping to take advantage of these capacities by isolating detoxification genes from pesticide-resistant insects, inserting them into bacteria, and growing the transgenic microbes in industrial fermentation vats to mass produce the enzymes. An alternative (but more difficult) approach might be to mass culture...

Chemical detoxification of bacterial exotoxins

Shortly after the determination that toxic components were associated with bacterial pathogens, several studies showed that cell extracts or cell cultures of a pathogen could be treated with chemical denaturants, such as formalin, to produce nontoxic immunogenic material that could prevent the disease associated with that pathogen. In the case of diphtheria toxin and tetanus toxin, chemical modification with formalin produced toxoids that were used as acellular vaccines in large-scale immunizations. This resulted in a remarkable decrease in the incidence of both diphtheria and tetanus within the populations that were immunized. In areas where these toxoids are not administered, diphtheria and tetanus remain clinically important diseases. In addition to formalin, other chemicals have been used to detoxify bacterial exotoxins, including glutaraldehyde and hydrogen peroxide. In contrast, the chemical toxoiding of other exotoxins, such as cholera toxin and pertussis toxin, has been more...

Alternative insemination See artificial insemination

Traditional ethnomedicinal systems are typically holistic, meaning that they aim to treat the whole person rather than a specific disease or symptom and that they therefore address not only the physical patient but also the mind and spirit. It is typically assumed that each individual possesses an innate healing capacity (an immune system in the broadest sense), and the goal of such treatment generally is to reinforce this, restoring strength and balance to weakened systems with a variety of natural modalities foods, herbs and other botanicals, body work, detoxification, and so on, tailored as much as possible for the individual. The

Mercury in the environment

In 1996 a team at the University of Georgia in Athens, USA, led by Richard Meagher, reported that they had genetically engineered plants that could detoxify land polluted with mercury compounds by absorbing them and reducing them to elemental mercury, which was then released from the plants' leaves. They had taken a gene from bacteria that can carry out this process and inserted it into a weed called arabidopsis, which was then shown to thrive on a growth medium that contained twice the level of mercury chloride that would kill normal plants.

Antifouling paint and toxic tin

Barnacles growing on the undersides of boats are a problem because they reduce the speed of the boat and can damage the hull. Pesticides (mol-luscicides) have, therefore, been developed to combat this. One is tributyl tin (TBT). Paints containing TBT were applied to the underside of boats to discourage the barnacles from growing on the surface of the hull. However, small quantities of the substance would dissolve from the paint and disperse in the surrounding water. The result was that the concentration of TBT in the water was sufficient to start poisoning other molluscs and marine organisms, especially in enclosed areas such as harbours. One particular victim was the dog whelk, which suffered not from lethal poisoning but from a bizarre effect whereby the females developed male characteristics, so affecting breeding. This effect is called imposex. It was found to occur after exposures as low as i nanogram per litre of water (a nanogram is i thousand millionth of a gram). Although...

Phase Ii Metabolizing Enzymes Glutathione Stransferases

The fate of the active intermediates of the Phase I reaction is governed by the Phase II detoxifying enzymes, like GSTs, in conjugation with glutathione or reduction reactions, resulting in less toxic and readily excreteable metabolites.32,34,36 It is assumed that GSTs are one of the major detoxification systems that protect cells from cytotoxic and carcinogenic insults.34,47 Therefore, the extent and duration of bioactivated toxic or carcinogenic compounds in an organ depend on the interplay of both biotransforming enzyme systems. Clearly, the yield of these metabolites would be higher if cells were rich in Phase I bioactivating enzymes, but poor on detoxifying Phase II enzymes.

Why do the different forms of mercury cause different effects

Although these initially detoxify the mercury, in the kidney they can degrade and the product mimics a natural substance which is transported into cells, where the attached mercury causes serious damage. The inorganic mercury does not, however, enter the brain as it cannot cross the so-called blood-brain barrier because it is not soluble in fat.

Miscellaneous Drugmetabolizing Enzymes

The microsomal epoxide hydrolase is involved in the first-pass metabolism of highly reactive epoxide intermediates and acts coordinately with CYPs (e.g., CYP 1A1 and CYP 1A2) to inactivate deleterious polycyclic hydrocarbon oxides and epoxides. The enzyme can also convert inactive diols to highly toxic and carcinogenic metabolites, thus exhibiting the same dual role of procarcinogen detoxification and activation found in CYPs.21,75,76 Only a few studies on the expression of epoxide hydrolase in the human pancreas are published. In one study, the expression of epoxide hydrolase was found only in acinar cells.77 NAD(P)H quinone oxido-reductase, an important enzyme in the activation and detoxification pathways of quinone compounds, sulfotrans-ferases, uridine diphosphate, and the flavin-containing monooxygenases, which are polymorphic,21 have been rarely or never described in the human pancreas.

Models For Toxicological Testing

Different factors are believed to influence the activity of drug-metabolizing enzymes, hampering meaningful comparisons between xenobiotic metabolism of animals and humans. These include age, sex, environmental exposure, diet, pathophysiological status, drug-drug interactions, and genetics (interindividual differences in the activity level of various isoforms, polymorphisms).2 Sex differences in the expression of CYPs within the same species have been shown for rat and mouse, whereas a sex specific human CYP isozyme has not yet been reported.3 Concerning environmental exposure, there is even little comparison between rats and mice (and between strains of the same species) with respect to chemical carcinoge-nicity and in the pathways for both activation and detoxification.2,4 Experimental models are kept in a controlled environment with a defined dose regimen and dietary restrictions, limiting the chance of drug-drug interactions whereas in humans, drug-metabolizing enzymes are...

The Role Of Cyp Enzymes In Other Diseases

Nijhoff et al.48 investigated the effect of the dietary, naturally occurring anticarcinogens flavone, coumarin, a-angelicalactone, and ellagic acid on the activity of GSTs in the esophagus, stomach, and pancreas of male Wistar rats. The treatment resulted in strong chemoprotective effects in the esophagus and stomach and, to a lesser extent, in the pancreas by enhancing the GST detoxification system. The lesser effect in the pancreas was explained with the shorter exposure time and intensity with the dietary substance.48 These findings are in line with reports of GST enzyme induction in the pancreas of rat after a diet rich in cruciferous vegetables.49

Treatment by the Psychiatrist with Medical Followup

The psychiatrist might recommend treatment on an inpatient basis. This is needed for severe depressions with suicidal thinking and is often necessary for schizophrenia with delusions and for hysteria when the patients behavior involves falling or an inability to walk or is associated with drug dependence and a need for detoxification. After discharge, such patients often need continued treatment by the psychiatrist with medical follow-up provided by the primary care physician.

How methylisocyanate kills its victims

In the lungs there is quite a lot of a sulphur containing substance called glutathione which functions to detoxify noxious chemicals. This can react with methylisocyanate and remove it. However it seems this detoxication is but a temporary respite because the product of this interaction carries the methylisocyanate away from the lungs to distant sites in the body such as the bones and muscles where it is released and causes damage. The detoxication product has been called a 'chemical taxi'.

Specific Hepatic Toxins

Acetaminophen is a popular over-the-counter pain reliever that also has anti-inflammatory and antipyretic properties. It is usually a safe drug unless taken in large quantity or when used by individuals whose alcohol drinking behavior is excessive. The mechanism of acetaminophen toxicity is an excellent example of liver pathology. Figure 7.5 shows the metabolism of acetaminophen. It is important to note that several metabolic fates are possible for acetaminophen but over 90 of the drug is excreted as conjugates with glucuronic acid or sulfate. In normal use, less than 5 of acetaminophen will be converted to a reactive electrophilic metabolite, N-acetyl-p-benzoquinoneimine (NAPQI). That portion which is converted to NAPQI will be inactivated readily by reduced glutathione under normal conditions. However, when NAPQI accumulates, it is toxic and binds to nucleophilic macromolecules in the hepatocyte causing cell necrosis. If high amounts of acetaminophen are ingested, then the...

Implementation of the Plan

Patients likely to experience withdrawal symptoms require detoxification. Past withdrawal symptoms are the best predictor of those in the future, Many patients will seek detoxification simply to gain temporary relief from their withdrawal misery, but not every patient should necessarily be detoxified simply because of an expressed desire to do so. Any patient who has never undergone medical detoxification should be given the opportunity as quickly as possible, as should anyone active in treatment who relapses. Medical detoxification should always be undertaken whenever a patient's alcohol or drug use significantly compromises the treatment of any other disorder (e.g., epilepsy, diabetes, cardiovascular dysfunction, anxiety and depressive disorders). Otherwise, detoxification should be undertaken only when part of a broader, mutually agreed-upon, long-range treatment strategy in order to deter poorly motivated patients from employing revolving door detoxification as a stopgap measure...

Preventive Maintenance

Successful completion of detoxification or a time-limited treatment program (e.g., 30 days of residential treatment) does not constitute cure an unfortunate assumption that most patients, their families, their employers, and all-too-many physicians make. It takes approximately two years for patients to establish a foothold on recovery, during which time they may have several relapses. In the first year, they must try to cope with the activities and stresses of everyday life not to mention a calendar of holidays, birthdays, and season-specific events without the use of alcohol or drugs. During the second year, they usually have a better idea of what to expect and what to do, having seen most situations at least once and tested various coping strategies. It is important for patients to see the primary care physician on a weekly basis, if only for five minutes or so, during the first several months after detoxification and then perhaps on a biweekly basis during the second six months....

Drug squad general practice

When I come across people who have taken drugs like heroin in the past, sometimes for quite long periods, I often ask them what made them stop. It turns out that this is rarely the result of drug treatment programmes, 'detoxification' or 'rehabilitation', but usually follows some wider change of lifestyle prompted by a new partner or a new job, a spell in prison or by simply getting bored with the drug scene. This confirms that when people really decide to stop, they just stop and often report relatively little difficulty in overcoming the much-publicised problems of physical and psychological dependency. Though the official drug misuse guidelines emphasise that methadone prescription 'should be seen as an enhancement to other psychological, social and medical interventions', I have become increasingly sceptical about the value of these initiatives.

Accumulation of Free Radicals OxidizedNitrosylated Proteins

A role in neurotoxicity in this model. Similar results were observed when UPS function was inhibited at the level of ubiquitination (39). Several other studies have demonstrated that proteasomal inhibition could exacerbate toxicity of oxidative stressors (34, 40-42). Not always is it clear however if the increase in toxicity is solely due to the impairment of degradation of oxidatively damaged proteins or if proteasomal inhibition in itself leads to oxidative injury. In a model using primary mesencephalic cell cultures epoxomicin did not have any effect on the direct increase of ROS, but led to an elevation of oxidized protein and increased neuronal vulnerability to normally subtoxic levels of several complex-I inhibitors which induce oxidative stress. This increase in toxicity was partially abrogated by antioxidants suggesting that in this model proteasomal inhibition reduced the cellular capacity to detoxify oxidized protein (42). In contrast, in a study by Kikuchi et al. (41)...

Cardiac Function And Toxicity General Principles

Cardiotoxicity can be both acute and chronic in nature. Acute cardiac injury carries a high risk because of the indispensable character of heart action. Mechanisms associated with chronic injury have become better understood in recent years. Aspects of chronic cardiac injury include alterations in myocardial cell excitability, activation of pre-toxins, failed chemical detoxification, accumulation of an active toxin, and extension of toxic pharmacological effects. Later in this chapter specific

Cytoplasmic determinants

Cytochrome P450 Cytochrome m CYP EC 1.14.14.1 Large group of mixed-function oxidases of the cytochrome b type, involved, among other things, in steroid hydrox-ylation reactions in the adrenal cortex. In liver they are found in the microsomal fraction and can be induced for the detoxification of foreign substances. Found in most animal cells and organelles, in plants and in microorganisms.

Metabolic transit and in vivo effects of Maillard reaction products

Much interest has been raised also by the possible activation of xenobiotic enzymes by MRPs. Induction of detoxifying enzymes, either by natural or synthetic substances, is still a promising chemopreventive strategy (Faist and Erbersdobler, 2001). Naturally occurring substances in foods have been shown to serve as antimutagens, which may function as chemical inactivators, enzymatic inducers, scavengers and antioxidants. The modulators can act through enzyme systems by inducing phase-I and phase-II enzymes or by altering the balance of different enzyme activities. Phase-I metabolic transformations include reduction, oxidation and hydrolytic reactions in order to release or induce functional or reactive groups from or into the xenobiotic substances. Phase-II transformations are mostly conjugation reactions of the parent xenobiotics, or phase-I metabolites, with sulphur-containing amino acids or glutathione. The conjugation reactions facilitate transport and hence elimination. Thus the...

Tobaccoderived Carcinogens 2231 Tobacco Components

Experiments with cultured human tissues and human liver and lung microsomes have pointed to carbonyl reduction as a major pathway of NNK metabolism.67,68 This metabolic conversion results in the formation of NNAL. NNAL and NNAL-Gluc have been detected in the urine of active smokers70 and passive smokers.71 Although glucuronidation is generally considered a detoxification pathway, its role in carcinogen delivery to target organs cannot be excluded. In fact, a-hydroxylation products, indicative of metabolic activation as described below, have been detected in rat urine after treatment with NNAL-Gluc.72 In the liver, for example, the glucuronidation process would enhance carcinogen elimination. However, in organs such as the colon, due to the presence of bacterial flora and the associated enzyme activity, NNAL-Gluc can be hydrolyzed to yield the parent nitrosamine by the action of p-glucuronidase. A similar process may occur in the pancreas because p-glucuronidase activity has, in fact,...

Phytoremediation of Organic Pollutants

Many plants come naturally well suited as environmental monitors and cleansers. Their root surfaces often are extensive and chemically sensitive, having evolved specifically to adsorb (accumulate on the outside) or absorb (take inside) nutrients from soils and waters. Most plants have innate systems for translocating, sequestering, and sometimes deporting (e.g., via transpiration or leaf fall) toxic foreign compounds. Plants collectively have huge biomass, making them potentially useful as repositories and or detoxifiers for vast amounts of pollutants. Plants in effect are self-powering systems, equipped with solar panels (leaves) that collect energy from natural sunlight. Finally, being sedentary and dependent on local environmental conditions, many plants have evolved genetic capabilities to detoxify or otherwise ameliorate the poisonous effects of numerous site-specific contaminants. Trichloroethylene (TCE), a toxic and carcinogenic industrial solvent, is a widely distributed...

Characterization of hazard in vitro

While in vitro experiments offer a partial solution to the safety evaluation of chemicals, they cannot completely replace animal experiments for this purpose. Many chemicals are poisonous because they affect organs or systems as well as, or rather than, individual cells. The human body, like that of any mammal, is a highly complex, integrated system and reacts to chemicals in many different ways, far more than can be predicted from one or two different types of isolated cells. Most of the cells in our bodies have some similarities (for example, they all have a nucleus), but brain cells are very different from muscle cells, otherwise we would not be able to think. Different types of cells have specialized functions which can make them a target for chemicals in specific ways. In particular, their metabolic capabilities are different and they may be unable to detoxify chemicals in the same way as liver cells, for example. This is illustrated by the story on p. 296. There is no doubt that...

Risk assessment of food contaminants

Many scientists have been increasingly unhappy with this approach as it has become apparent that there are a number of mechanisms by which chemicals can cause cancer. Even with the chemicals that damage DNA and cause mutations we now know that the damage can be repaired, that cells with damaged DNA are removed by apoptosis, that much of the DNA is redundant, and that a damaged cell must divide in order to become a tumour. Altered cells (that is, cancer cells), moreover, can be removed by the immune system. Furthermore, in order to cause cancer, a chemical has to get inside a cell in the body, and the body has many barriers against chemicals entering it, for example the membranes of cells form a natural barrier the blood is able to remove and eliminate chemicals into the urine and the body has systems to pump chemicals out of cells, and metabolism to detoxify them. The scenario of chemicals entering a body and causing toxic effects can be likened to a few soldiers trying to get into...

Endogenous Substances Toxic To Pancreatic Pcells

Increased free fatty acid (FFA) levels can also induce apoptosis in pancreatic p-cells,212,213 as can elevated glucose levels.214,215 Hence, a glu-colipotoxicity hypothesis has also been proposed,205,216 suggesting that the toxic actions of elevated FFAs on various tissues will become particularly apparent in the context of hyperglycemia. It is believed that high glucose decreases fat oxidation and consequently the cellular detoxification of fatty acids. Thus, glucose induces and activates enzymes and transcription factors involved in fat synthesis and storage and simultaneously switch off fat oxidation via the accumulation of Malonyl-Coenzyme A.217,218 In a recent study, it has been shown that elevated glucose and FFAs together induce cell death by apoptosis in both rat and human islet p-cells with a marked synergistic effect.219

Functions And Biological Activities Of Lipopolysaccharides

Circulating LPS molecules naturally form micellar aggregates and a variety of host LPS binding proteins are important in mobilizing LPS monomers from such complexes. These include BPI (see previous discussion) and LPS-binding protein (LBP), a 60 kDa acute-phase protein produced by hepatocytes. One role of these proteins is to clear and detoxify LPS. For example, LBP is known to transfer LPS to high-density lipoprotein fractions. However, LBP is also a crucial component of the signaling pathway through which animal cells are stimulated to produce cytokines and inflammatory mediators.

Pharmacogenomics and Cancer

The interplay between the patient host and tumor is another level of complexity that is just beginning to be explored. What is clear is that the contributions of the tumor and host must both be accounted for in predicting the effects of prescribing a certain drug (Fig. 1). Adverse drug responses, which usually involve enzymes localized in the liver, are, by and large, a host response. Drug response can be mediated by both host and tumor for example, drug detoxification by the host might decrease response, whereas protein present in the tumor might affect drug availability. The aggressiveness of the tumor, which greatly influences the therapeutic regimen the oncologist chooses, is largely tumor-defined.

Personalized Medicine for Pain Management

Eventually it became known that the patient was receiving opioid medications from other physicians. He was informed of the situation and offered several options, including counseling and detoxification programs, but chose to seek another physician. He did return to the practice briefly, but subsequently failed to return after another scheduled operation.

Induction of PAC Vesicles in Vegetative Tissues

The PAC vesicles does not permit the detoxification of this herbicide. Phos-phinothricin acetyltransferase molecules are bound in the aggregates within the PAC vesicle, which obviously causes the loss of enzyme activity. The transgenic plants will become resistant to phosphinothricin if a mutation of a gene results in an alternative subcellular localization of the fusion protein. Such mutants should provide a clue to understanding the molecular mechanism involved in the biogenesis of the PAC vesicles from the ER.

Arsenic in drinking water

So what can the people of this region do One answer is to dig deeper wells that go below 200 m or shallower wells that reach down only 20 m. In this way the contaminated layer of ground water can be avoided. Once the population has access to uncontaminated water then the arsenic in their body is quickly lost indeed giving them anti-arsenic chelating agents is not necessary because the body will detoxify itself. Those who display the skin conditions associated with arsenic can be treated with lotions and antibacterial ointments and slowly the condition will improve. The Indian government has issued chlorination tablets that will oxidize the arsenic in water, converting it from AsO33- to AsO43-, which forms an insoluble salt with the iron which is also present in the water.

Multidrug Resistance1 Gene

Cancers treated with multiple anticancer drugs tend to develop or display cross-resistance to many other chemotherapy agents to which they have never been exposed. Several mechanisms contribute to the development of such multidrug resistance, including increased drug efflux from the cell by membrane transporters, activation of drug detoxification enzymes such as glutathione-S-transferase, decreased drug uptake into the cell, and defective apoptotic pathways (reviewed in ref. 23).

Middle Aged Alcoholic with Jaundice and Ascites

A 51-year-old white male came to the Emergency Department complaining of weakness, lack of appetite, shortness of breath, and abdominal distension. He was a known alcoholic who had failed detoxification programs several times in the past and continued to drink approximately one pint of vodka or gin per day. Eight months before presentation he had been admitted to another hospital with alcoholic hepatitis and at that time had suffered severe withdrawal symptoms. Soon after discharge, however, he resumed drinking. Two weeks prior to the current presentation, he developed a cold and lost his appetite. He began taking over-the-counter ibuprofen for non-specific pains and continued to drink. When he experienced profound weakness, shortness of breath, and abdominal bloating, he asked his girlfriend to take him to the hospital.

The Chromium Glucose Tolerance Factor

Cr6+ or Cr3+ result in greater amounts of LMWCr3+, while injections of Cr at more physiologically relevant levels favor binding by high molecular weight proteins 44 . This supports the original interpretation that LMWCr is involved in the detoxification of excessive absorbed chromium 35 , and is less consistent with the assumption that LMWCr is the relevant form through which Cr3+ carries out its role as an essential metal in humans.

Phytoremediation of Mercury Poisons

How might biotechnology help clean up mercury spills Researchers at the University of Georgia think they have an answer in transgenic plants engineered to detoxify mercury's more poisonous forms. Experimental mustard plants were modified to carry two genes of bacterial origin merA, which converts Hg(II) to Hg(0), and merB, which degrades MeHg to methane and Hg(II). Hg(0) is a relatively benign form of mercury 100-fold less toxic than Hg(II) that the GM plants either sequester in their tissues or volatilize into the atmosphere as they transpire water vapor through surface pores. Due to their newly acquired metal-detoxification systems, these transgenic plants can

Accelerated Directed Evolution

In 1994, it occurred to Willem Stemmer that genetic engineers might be able to speed up the commercial development of drugs and vaccines by imitating nature's ingenuity. In an experimental test of this idea using the prokary-otic bacterium Escherichia coli, Stemmer digested the TEM-1 gene (which codes for an enzyme that breaks down the antibiotic cefotaxime) into small fragments and then randomly reassembled the pieces into full-length DNA sequences. He called this procedure in vitro DNA shuffling, and it was indeed rather analogous to shuffling a deck of cards repeatedly. The reassorted DNA sequences then were inserted into legions of bacteria and tested for capacity to confer tolerance to cefotaxime (the selective agent). After just a few rounds (generations) of this evolution-mimicking process, Stemmer created novel TEM-1 enzymes that could detoxify a 32,000-fold higher concentration of cefotaxime than did the originals. In effect, by generating genetic variety by molecular...

The development of an antidote

Knowledge that paracetamol was detoxified by the thiol glutathione led the development of an antidote. Glutathione itself cannot be given to the patient after an overdose, so a number of similar substances were initially tried as possible antidotes. There was some success but some had unpleasant effects. It was then found that a substance called N-acetylcysteine would help to regenerate the glutathione in the liver. Barbiturates and alcohol both increase the activity of (induce) the enzymes that metabolize paracetamol to the toxic product. A chronic alcoholic or someone who has been prescribed barbiturate drugs will be at greater risk when taking more than the recommended dose of paracetamol because a greater proportion of the dose will be converted into the toxic product. It would be equivalent to taking a larger dose. In the case of an alcoholic the liver may already be compromised by repeated and long-term alcohol abuse and so be more vulnerable and less able to detoxify...

Susceptibility To Environmental Toxins

A number of gene families determine the individual cellular settings of detoxifying enzymes and a person's capacity for enzymatic detoxification (see Chapter 7). This accounts for both an individual's susceptibility to environmental toxins and a predisposition for the development of environment-related diseases. The human super gene family of uridine 5'-diphosphate glucuronyl-transferases (UGT) is known to represent Phase II detoxifying enzymes that glucuronidate not only dietary by-products and endogenous metabolites, but also therapeutic drugs or polycyclic hydrocarbons and heterocyclic amines, which are known mutagens. The consequence of an impaired Phase II metabolism is an accumulation of cyto-and genotoxic xenobiotics that are generated by an adduct reaction with continuously produced reactive oxygen species from oxidative Phase I metabolic enzymes. The UGT1A7 gene encodes one specific UGT isoform that has been shown to glucuronidate several known carcinogens, including those...

Structure and function

Without the liver, survival is measured in hours, and no artificial system has yet been devised to substitute for hepatic function. The liver is the largest solid organ in the body and its essential functions include regulation of protein, fat and carbohydrate metabolism, synthesis of plasma proteins, ketones and lipoproteins, and detoxification and excretion. Via the hepatic portal circulation it receives and filters the entire venous drainage of the spleen, gastrointestinal tract and pancreas. Through the production of bile, it is also essential for digestion and absorption, particularly of dietary fats and fat-soluble vitamins.

A possible mechanism underlying the toxic oil syndrome

Research on the victims of the poisoning also found that they were more likely to have a deficiency in an enzyme, N-acetyltransferase, than those who did not suffer the effects. This enzyme detoxifies aniline and similar chemicals. There is a known genetic variation in the ability to acetylate in the human population, with about half the European population showing a relative deficiency in this enzyme (see pp. 29-31, 70, for more on this). Such individuals, known as slow acetylators, would be less able to detoxify the aniline. This could account for the variability in susceptibility, whereby some individuals consumed contaminated oil but did not suffer toxic effects.25

Lowmolecularweight Chromiumbinding Substance Lmwcr

Low-molecular-weight chromium-binding substance is a naturally occurring oligopeptide composed of glycine, cysteine, aspartate, and glutamate with the carboxy-lates comprising more than half of the total amino acid residues 176, 177 . Despite its small size (approximately 1500 molecular weight), the molecule tightly binds four equivalents of chromic ions. By 1995 the oligopeptide had been isolated and purified from the liver of rabbit 176 , and partially purified from the livers of dog 178 and mouse 177 . A related chromium-containing oligopeptide from bovine colostrum (M-LMWCr) is comprised of the same amino acids but in distinctly different ratios and also stimulates insulin-dependent glucose metabolism in rat adipocytes 172, 174 . Whether the oligopeptide is present in other forms of milk is unknown. The significance of these differences between the liver and the colostrum oligopeptides is essentially unexplored. The oligopeptide is isolated as the holo-oligopeptide (so that it may...

Biochemistry

The behavior of a substance in a biological system depends to a large extent upon whether the substance is hydrophilic (water-loving) or hydrophobic (water-hating). Some important toxic substances are hydrophobic, a characteristic that enables them to traverse cell membranes readily. Part of the detoxification process carried on by living organisms is to render such molecules hydrophilic, therefore water soluble and readily eliminated from the body.

Pulmonary Exposure

The major function of the lungs is to exchange gases between the bloodstream and the air in the lungs. This especially includes the absorption of oxygen by the blood and the loss of carbon dioxide. Gas exchange occurs in a vast number of alveoli in the lungs, where a tissue the thickness of only one cell separates blood from air. The thin, fragile nature of this tissue makes the lungs especially susceptible to absorption of toxicants and to direct damage from toxic substances. Furthermore, the respiratory route enables toxicants entering the body to bypass organs that have a screening effect (the liver is the major screening organ in the body and it acts to detoxify numerous toxic substances). These toxicants can enter the bloodstream directly and be transported quickly to receptor sites with minimum intervention by the body's defense mechanisms.

Problem Areas

Substances like ethanol (CYP 2E1) and caffeine (CYP 1A2) usually results in their detoxification or inactivation.8,9,13,20,85 However, this detoxification depends on the availability and capability of the Phase II conjugating system, like GSTs. The depletion of these enzymes results in a higher concentration and prolonged effect of CYP-activated toxic substances. Besides giving a risk estimation or prediction for pancreatic disease development, the investigation of drug-metabolizing enzymes might give some insight into the pathophysiological mechanisms and could improve the understanding of the biology or, even perhaps, the etiology of the diseases. Considering the blood supply of the pancreas, where a portion of arterial blood passes through to the islets before nourishing the exocrine pancreas,101 the expression and apparently the higher concentration of most of these enzymes in islet cells in humans and animals (Chapter 8)3,40,102,103 is understandable. The islet cells are the...

Cholestasis

This is the deposition of fibrous tissue, collagen, usually on a chronic basis, in various parts of the liver. As the normal hepatocytes are replaced by collagen there is a progressive impairment in liver functions such as drug detoxification and other hepatic metabolic processes. Blood and biliary flow also are affected. The best example of a toxicant causing cirrhosis is ethyl alcohol, although other chemicals may also cause this disorder. There is no specific chemical test for cirrhosis. The diagnosis is suspected on the basis of the patient's history and can be confirmed by microscopic evaluation of a needle biopsy.

Closure on a Plan

Once physician and patient have agreed on the diagnosis, they should immediately close on a coherent, stepwise treatment plan. At every stage of treatment, there should be agreement on a backup plan (e.g., inpatient detoxification) if the first plan (e.g., outpatient detoxification) fails. Involvement of immediate family members, close friends, or both is important not only at this point, but also at every treatment stage.

Hepatocytes

In the adult liver, hepatocytes mainly fulfil metabolic functions such as the production of albumin, regulation of glucose and lipid metabolism, detoxification and production of bile acid, but appear to have little involvement in immunoregulatory processes. Although hepatocytes express TLR2 and TLR4 receptors and are responsive to LPS, this response is fairly weak with only two-fold elevated levels of serum amyloid A (SAA) after LPS 28 . Similarly, stimulation with the TLR2 ligand bacter

Relapse Management

A supervised environment, free from drink or drugs. A structured daily routine should be restored and appropriate social roles reinstated as soon as possible. Such swift and definitive measures can prevent the need for detoxification or a residential treatment program. With proper relapse management, the patient rapidly can resume the preventive maintenance mode, now buttressed against contingencies that previously had gone unanticipated or uncountered.

Toxicity

Genetic differences in both the patient host and the tumor contribute to variable responses to therapy and to different clinical outcomes. Effective therapies must encompass prognostic and predictive elements of both the host's (the patient's) and the tumor's genomes. Toxicity is principally a host response involving liver-localized enzymes. The aggressiveness of the tumor is principally tumor-defined. Drug response can be mediated both by involving host detoxification metabolism and tumor-governed drug availability.

Aflatoxin

Most manufacturing processes do not detoxify aflatoxin and therefore if the aflatoxins are not detected, products will be marketed. One of the processes used for reducing aflatoxin levels is nixtamalization (alkaline cooking), which is used during the making of corn tortillas, tortilla chips, and corn chips, and gives a 51 to 78 reduction in aflatoxin levels (Torres et al., 2001).

A cautionary tale

A new drug was being tested at a pharmaceutical company. The first tests were carried out in isolated liver cells in vitro, and the drug was found to be not toxic to these cells. The drug was then given to experimental animals, in which it caused the destruction of the adrenal glands (which are found close to the kidneys). When cells from the adrenal gland were used instead of liver cells in in vitro tests, they were, as expected, destroyed. This was because the cells from the adrenal gland were not able to detoxify the drug whereas the liver cells were. If the ability of the liver cells to detoxify the drug were blocked, they too became susceptible to the toxic effect of the drug. Liver cells are the cells most often used in vitro because they are the easiest to prepare and use. They are also often the most readily available kinds of human cell. The toxicity illustrated by this example could easily occur in humans if isolated cells alone were used to test new chemicals.

Metals

Lead is a heavy metal which is taken up by proximal tubule cells. Within these cells lead interferes with mitochondrial biochemistry. The cell has some ability to detoxify lead and appears to do this to some degree by forming inclusion bodies of lead bonded to acidic proteins. Such bodies, which appear before lead toxicity starts, may be seen as microscopic inclusions within the cell.

Home Detox

Home Detox

Never before revealed. Home Detox - Step By Step Guide To Dextoxify The Body. Has too much late night behavior and partying got you feeling bad about yourself? Are you trying to lose weight but nothing is happening? Maybe you are just sick of all of the toxins that are in the air you breathe, the water you drink and the foods you eat. If so, then you need to do something about it. If you find yourself feeling bad about your health, there are ways that you can help your body right at home.

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