Cysteine metabolism and
metal toxicity
Quig D. [Altern Med Rev 1998 Aug;3(4):262-70] The pro-oxidative effects of
metals are compounded by the fact that the metals also inhibit antioxidative
enzymes and deplete intracellular glutathione. Cysteine has a pivotal role in
inducible, endogenous detoxication mechanisms in the body, and metal exposure
taxes cysteine status. Basic research pertaining to the transport of toxic
metals into the brain is summarized, and a case is made for the use of
hydrolyzed whey protein to support metal detoxification and neurological
function. Early detection and treatment of metal burden is important for
successful detoxification, and optimization of nutritional status is paramount
to the prevention and treatment of metal toxicity.
Mechanism of action and value of N- acetylcysteine in the treatment of early and
late acetaminophen poisoning: A critical review.
Jones AL. [Journal of Toxicology -- Clinical Toxicology. 1998; volume 36,
number 4, pages 277-285] The mechanism of action of N-acetylcysteine in early
acetaminophen poisoning is well understood, but much remains to be learned of
the mechanism of its possible benefit in acetaminophen poisoning presenting
beyond 15 hours. Candidate mechanisms for a beneficial effect in-clude
improvement of liver blood flow, glutathione replenishment, modification of
cytokine production, and free radical or oxygen scavenging.
Glutathione deficiency in alcoholics: risk factor for paracetamol hepatotoxicity.
Lauterburg BH and Velez ME. [Gut. 1998; volume 29, pages 1153-1157]. "The
data indicate that low glutathione may be a risk factor for [acetaminophen]
hepatotoxicity in alcoholics because a lower dose of [acetaminophen] will be
necessary to deplete glutathione below the critical threshold concentration
where hepatocellular necrosis starts to occur."
Chronic ethanol and nicotine interaction on rat tissue antioxidant defense
system.
Husain K, Scott BR, Reddy SK, Somani SM. [Alcohol. 2001 Oct;25(2):89-97.]
This study was undertaken to examine the interactive effects of chronic ethanol
and nicotine consumption on the antioxidant defense system in different tissues
of rat. Chronic ingestion of ethanol resulted in a significant depletion of
glutathione (GSH) content in liver, lung, and testes, whereas chronic
administration of nicotine significantly depleted GSH content in liver and
testes. The combination of ethanol plus nicotine resulted in a significant
depletion of GSH content in liver, lung, and testes. Chronic ingestion of
ethanol resulted in a significant decrease in glutathione peroxidase (GSH-Px)
activity in liver and kidney, whereas a combination of ethanol plus nicotine
increased GSH-Px activity in liver and decreased GSH-Px activity in kidney and
testes. Ethanol, nicotine, or a combination of ethanol plus nicotine
significantly increased lipid peroxidation, respectively, in liver. It is
suggested that prolonged exposure to ethanol and nicotine produce similar,
and in some cases additive, oxidative tissue injuries in rat.
Treatment of sulfur mustard (HD)-induced lung injury.
Anderson DR, Byers SL, Vesely KR. [J Appl Toxicol 2000 Dec;20(S1):S129-S132]
An in vivo sulfur mustard (HD) vapor exposure model followed by bronchoalveolar
lavage was developed previously in this laboratory to study biochemical
indicators of HD-induced lung injury. This model was used to test two treatment
compounds-niacinamide (NIA) and N-acetyl cysteine (NAC)-for their ability to
ameliorate HD-induced biochemical changes. These results show that NAC may be
useful as a potential treatment compound for HD-induced lung injury.
Role of glutathione redox cycle and catalase in defense against
oxidative stress induced by endosulfan in adrenocortical cells of rainbow trout
(Oncorhynchus mykiss).
Dorval J, Hontela A. [Toxicol Appl Pharmacol. 2003 Oct
15;192(2):191-200.]
The role of
antioxidants in maintaining the functional integrity of adrenocortical cells
during in vitro exposure to endosulfan, an organochlorine pesticide, was
investigated in rainbow trout (Oncorhynchus mykiss). ...protection against the
adrenal toxicity of endosulfan, a pesticide that impairs cell viabilityand
cortisol secretion. CAT, GPx, and GSH were identified as important antioxidants
in maintaining the function and integrity of rainbow trout adrenocortical cells
and ATA, L-BSO, and NAC were identified as effective modulators of CAT and GSH
redox cycle. Moreover, this study suggests that the glutathione redox cycle may
be more efficient than catalase in protecting adrenocortical cells against
endosulfan-induced oxidative stress.
Toxic metals and
antioxidants: Part II. The role of antioxidants in arsenic and cadmium toxicity
Patrick L. [Altern Med Rev. 2003 May;8(2):106-28.] Exposure to toxic
metals has become an increasingly recognized source of illness worldwide. Both
cadmium and arsenic are ubiquitous in the environment, and exposure through food
and water as well as occupational sources can contribute to a well-defined
spectrum of disease. The mechanisms of arsenic- and cadmium-induced damage
include the production of free radicals that alter mitochondrial activity and
genetic information. The metabolism and excretion of these heavy metals depend
on the presence of antioxidants and thiols that aid arsenic methylation and both
arsenic and cadmium metallothionein-binding. S-adenosylmethionine, lipoic acid,
glutathione, selenium, zinc, N-acetylcysteine (NAC), methionine, cysteine,
alpha-tocopherol, and ascorbic acid have specific roles in the mitigation of
heavy metal toxicity. Several antioxidants including NAC, zinc, methionine, and
cysteine, when used in conjunction with standard chelating agents, can improve
the mobilization and excretion of arsenic and cadmium.
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