Glutathione and Detoxification
The glutathione system is the body's primary detoxification mechanism and, as such, is responsible for the removal of toxic compounds from the body, regardless of their etiology. Heavy metals, pharmaceuticals, insecticides, cigarette toxins, air and water pollutants - just to name a few. If your body's intracellular glutathione level is not optimized, it logically follows that cellular damage will result. The cumulative damage caused by the relentless onslaught of environmental toxins defines the very process of aging and disease.
The following abstracts contain overviews of studies performed that demonstrate glutathione's role in detoxification. Click on the corresponding link (blue) to read the abstract as found on the National Institute of Health's government website:
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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