Liver toxicity alcohol

A number of substances including ethanol, isopropyl alcohol, polybrominated biphenyls, phenobarbital, and benzo( )pyrene have been shown to synergistically affect carbon tetrachloride toxicity." Alcohol has been a concomitant factor in many of the human cases of poisoning, especially in cases in which severe liver and kidney damage have occurred. Some substances such as chlordecone greatly potentiate the toxicity of carbon tetrachloride at... 

An excellent brief article on buprenorphine treatment has been provided by Taikato et al. (2005), which notes the common possible side-effects (headaches, nausea and vomiting, sweating, constipation, etc.) and drug interactions. The limited central depressant effect of buprenorphine may be compounded by alcohol and antidepressants, while the metabolism of buprenorphine can be enhanced by anticonvulsants, with therefore possibly reduced efficacy. There have been some case reports of liver toxicity from buprenorphine that is reversible if the medication is stopped (Herve et al. 2004), and often clinical guidelines will recommend that liver function tests are included in buprenorphine treatment, as they definitely should be with naltrexone. 

Naltrexone Nonselective competitive antagonist of opioid receptors Reduced risk of relapse in individuals with alcoholism Available as an oral or long-action parenteral formulation Toxicity Gastrointestinal effects and liver toxicity will precipitate a withdrawal reaction in individuals physically dependent on opioids and will prevent the analgesic effect of opioids... 

An example of a structural substituent that is often metabolized (bioactivated) to an electrophile is the allyl alcohol substituent (C=C—C—OH). Allyl alcohol moieties are found in many commercial chemical substances, either as the free alcohol or as an ester or ether. As illustrated in Scheme 4.1, allyl alcohols (and also as their esters or ethers) that contain at least one hydrogen atom on the alcoholic carbon can be oxidized in the liver by alcohol dehydrogenase (ALDH) to the corresponding a, 3-unsaturated carbonyl metabolite, which is toxic in many cases [29-31]. The hepatotoxicity of allyl alcohol (1), for example, is due to its oxidation by ALDH to acrolein (2), an a,(3-unsaturated aldehyde, which undergoes Michael addition with cellular nucleophiles in the liver [29] (Scheme 4.1). Cyclic allyl alcohols (Scheme 4.1) are expected to undergo similar enzymatic oxidation to yield a,(3-unsaturatcd carbonyl metabolites and are also likely to be toxic. 

Ethylene glycol is used as a freezing-point depressant in automotive antifreeze. It is highly toxic because the enzyme alcohol dehydrogenase and the coenzyme nicotinamide adenine dinucleotide (NAD) oxidize ethylene glycol to much more liver-toxic compounds like glyoxal, hydroxyacetaldehyde, glyoxylic... 

Toxic effects to the liver are studied under the topic of hepatotoxicity, and substances that are toxic to the liver are called hepatotoxins. Much is known about hepatotoxicity from the many cases of liver toxicity that are a manifestation of chronic alcoholism.6 Liver injury from excessive alcohol ingestion initially hampers the ability of the organ to remove lipids, resulting in their accumulation in the liver (fatty liver). The liver eventually loses its ability to perform its metabolic functions and accumulates scar tissue, a condition known as cirrhosis. Inability to synthesize clotting factors can cause fatal hemorrhage in the liver. 

EME and BEG, which is mainly obtained by enzymatic hydrolysis, represents respectively the 32-49 % and 29 45 % of total urinary metabolites cocaine can be converted, in small amounts, to norcocaine (NCOC) and psychoactive metabolite norbenzoylecgonine (NBE). The combined intake of alcohol and cocaine determines the formation of a pharmacologically active metabolite, the cocaethylene (ethyl ester of benzoylecgonine, CE), with a significant liver toxicity [13],... 

Kaviarasan, S. and Anuradha, C.V. (2007) Fenugreek seed polyphenols protect liver from alcohol toxicity a role on hepatic detoxification system and apoptosis. Pharmazie 62, 299-304. 

Kaviarasan, S., Ramamurty, N., Gunasekaran, P., Varalakshmi, E. and Anuradha, C.V. (2006) Fenugreek (Trigonella foenum graecum) seed extract prevents ethanol-induced toxicity and apoptosis in Chang liver cells. Alcohol and Alcoholism 41 (3), 267-273. 

Although it is the least toxic alcohol, ethanol is still a poisonous substance. When someone is suffering from a mild case of ethanol poisoning, we say that he or she is intoxicated. Animals often consume food that has fermented and contains alcohol. Their bodies must detoxify any alcohol in the food to keep it from building up in the blood and poisoning the brain. To detoxify ethanol, the liver produces an enzyme called alcohol dehydrogenase (ADH). 

Thiamine is given for alcohol-induced liver toxicity (to prevent Wernicke s encephalopathy). 

Used in mild-to-moderate pain May use in conjunction with opioid agents to decrease doses ot each Regular alcohol use and high doses of acetaminophen may result in liver toxicity Care must be exercised to avoid overdose when combination products containing these agents ate used Drug ot choice in severe pain Use immediate-release product with SR product to control breakthrough pain in cancer patents... 

ALCOHOL METHOTREXATE t risk of liver damage/toxicity Additive liver toxicity Be aware advocate abstinence. Monitor liver function... 

ALCOHOL KETOCONAZOLE May T risk of liver damage. Symptoms of nausea, headache, flushing and discomfort (similar to a disulfiram-type reaction) may occur Additive liver toxicity Be aware... 

Liver function is often abnormal in chronic inhalant abusers. After abstinence, function usually returns to normal, but if the individual returns to inhalant use, the problems will return. When inhalant use is coupled with alcohol abuse, which also causes liver toxicity, additive effects may occur. 

In a meta-analysis of 636 patients from 15 studies, who took chronic low-dose methotrexate for rheumatoid arthritis or psoriasis, the risk of liver toxicity increased with cumulative dose and heavy alcohol intake (56). 

A special mention of interaction of acetaminophen with alcohol consumption is warranted. Large numbers of reports in scientific literature and public media suggest that a potentially high risk of liver toxicity due to acetaminophen exists when consumed following alcohol intake. In a recent review, however. Dr. Barry Rumack suggests that only chronic heavy drinkers may be at greater risk following an overdose of acetaminophen and that no potentiation of toxicity occurs at therapeutic doses. 

Elevated liver enzymes may occur in up to 15% of patients cirrhosis is rare. Liver function tests, aspartate aminotransferase (AST) or alanine aminotransferase (ALT), should be performed periodically. Methotrexate should be discontinued if these test values show sustained results greater than twice the upper limits of normal. Serum albumin levels also should be checked periodically, as signs of liver toxicity in some patients may not have liver inflammation manifested by AST or ALT elevation. Liver biopsy is now recommended before beginning methotrexate therapy only for patients with a history of excessive alcohol use, ongoing hepatitis B or C infection, or recurring elevation of AST. Biopsies during methotrexate therapy are recommended only for patients who develop consistently abnormal liver function tests. ... 

A Dermatitis, night blindness, keratomalacia, xerophthalmia Serum vitamin A Teratogenic effects, liver toxicity with excessive intake alcohol intake, liver disease, hyperlipidemia, and severe protein malnutrition increase susceptibility to adverse effects of high intake , 6-carotene supplements recommended only for those at risk of deficiency (fat malabsorption)... 

One biological reaction that involves radicals is the one responsible for the conversion of toxic hydrocarbons to less toxic alcohols. Carried out in the liver, the hydroxyl-ation of the hydrocarbon is catalyzed by an iron-porphyrin-containing enzyme called cytochrome P450 (Section 12.8). An alkyl radical intermediate is created when Fe O abstracts a hydrogen atom from an alkane. In the next step, Fe OH dissociates homolytically into Fe and HO, and the HO immediately combines with the radical intermediate to form the alcohol. 

R. G. Thurman (1997). Gadolinium chloride blocks alcohol-dependent liver toxicity in rats treated chronically with intragastric alcohol despite the induction of CYP2E1. Mol. Pharmacol. 51, 944-950. 

LIVER Ethanol produces a constellation of dose-related deleterious effects in the liver. The primary effects are fatty infiltration of the liver, hepatitis, and cirrhosis. Because of its intrinsic toxicity, alcohol can injure the liver in the absence of dietary deficiencies. The accumulation of fat in the liver is an early event and can occur in normal individuals after the ingestion of relatively small amounts of ethanol. This accumulation results from inhibition of both the tricarboxylic acid cycle and the oxidation of fat, in part, owing to the generation of excess NADH produced by the actions of ADH and ALDH (see Figure 22-1). 

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