Over 135,000 scientific articles have described the impact of glutathione. The health conditions listed below are impacted by low glutathione. Click on a condition to read more. Information about the research can be found on the U.S. National Institutes of Health (NIH) digital archive of biomedical journals, www.pubmed.gov
- Whether accidental or intentional, acetaminophen poisoning is not uncommon; in fact, it is the most common drug- induced cause of liver failure. When hepatic glutathione is depleted, the toxic metabolite NAPQI fails to be conjugated and causes hepatic injury. At risk are chronic alcoholics, binge drinkers, patients taking medications that induce the P-450 isoenzyme system, and those with concomitant liver disease. PMID: 10223088
- Our findings suggest that acetaminophen administration selectively depletes (within 2 hr) mitochondrial glutathione, and produces local toxicity by altering membrane permeability and decreasing the efficiency of oxidative phosphorylation. This renders mitochondria more susceptible to oxidative damage… PMID: 8937421
- Toxic doses of paracetamol deplete intracellular GSH and result in cell death by a combination of mechanisms, leading to necrosis and apoptosis, mainly in the liver. In clinical situations characterized by low GSH, the risk of toxicity from therapeutic doses of paracetamol may conceivably be increased. This toxicity has been reported in chronic alcoholics who have low intrahepatic GSH and who may have an induced enzyme system that generates the toxic metabolite of paracetamol. PMID: 11941382
- In one study it was shown that the concentration of glutathione was decreased in red blood cells from male Alzheimer’s disease patients compared with age- and gender-matched controls. PMID: 15693022
- It has been observed that Alzheimer’s patients show an increased level of plasma TBARS, which indicates a higher free radical oxidation of plasma unsaturated phospholipids, and an increased oxidation of red blood cells glutathione, which indicates oxidative stress in peripheral cells. This latter, glutathione oxidation, was found to correlate statistically with the cognitive status of the patients. PMID: 15051321
- GSH is the most abundant cellular non-protein thiol, serves as an important antioxidant, and has been proposed to be important in the protection of cerebrum from oxidative damage. GSH has been reported to be decreased in cerebrum of aging rodents and humans (Hazelton and Lang 1980; Chen et al. 1989; Ravindranath et al. 1989; Iantomasi et al. 1993; Favilli et al. 1994; Martinez et al. 1995; Liu 2002), and alterations in GSH metabolism have been described in diseased regions of brain from AD patients (Aksenov and Markesbery 2001). Alterations in peripheral GSH metabolism have also been described in patients with mild cognitive impairment and AD. PMID: 15857408
- The most abundant endogenous antioxidant, glutathione, plays a significant role in combating oxidative stress. The ratio of oxidized to reduced glutathione is utilized as a measure of intensity of oxidative stress. Antioxidants have long been considered as an approach to slow down AD progression. PMID: 22015471
- In summary, the cerebral GSH and plasminogen systems are essential biological processes that combat the neurodegenerative processes that occur more significantly with advancing age. With knowledge of the physiopathology of neurodegenerative processes, both of these systems can be pharmacological targets, providing reason for hope of prevention of neurodegenerative diseases such as AD. PMID: 23650462 Read this article.
- Recent evidence suggests that some autistic children may have reduced detoxification capacity and may be under chronic oxidative stress. Based on reports of abnormal methionine and glutathione metabolism in autistic children, it was of interest to examine the same metabolic profile in the parents. The results indicated that parents share similar metabolic deficits in methylation capacity and glutathione dependent antioxidant/detoxification capacity observed in many autistic children. Studies are underway to determine whether the abnormal profile in parents reflects linked genetic polymorphisms in these pathways or whether it simply reflects the chronic stress of coping with an autistic child. PMID: 18512136
- This study looked at the metabolism of autistic children. Impairments in the methylation cycle, a very critical part of our body’s functioning, were found. Because of this problem in the methylation cycle, autistic children are predisposed to low glutathione which prevents them from detoxifying normally. It was also found that certain co-enzymes, all non-pharmaceutical, support that cycle. PMID: 15585776
- The induction of NK cell activity by IL-2, IL-15 and glutathione was more pronounced in a subgroup with very low NK cell activity. We conclude that that 45% of a subgroup of children with autism suffers from low NK cell activity, and that low intracellular levels of glutathione, IL-2 and IL-15 may be responsible. PMID: 18929414
- Purpose: We performed a randomized, double-blind, placebo-controlled trial to assess the efficacy of glutathione (GSH) in the prevention of oxaliplatin-induced neurotoxicity. Conclusion: This study provides evidence that GSH is a promising drug for the prevention of oxaliplatin-induced neuropathy, and that it does not reduce the clinical activity of oxaliplatin.
PMID: 12177109 - Background: Early clinical trials have suggested that glutathione (GSH) offers protection from the toxic effects of cisplatin. Conclusions: The results demonstrate that adding GSH to CDDP allows more cycles of CDDP treatment to be administered because less toxicity is observed and the patient’s quality of life is improved. PMID: 9261526
- Here we report that glutathione (GSH) plays a critical role in activation of apoptosis pathways by CD95 (APO-1/Fas) or anticancer drugs. We conclude that dominant apoptosis resistance depends, at least in part, on intracellular GSH levels, which may affect apoptosis signaling at different compartments, for example, the death receptor or mitochondria. PMID: 15105835
- Glutathione (GSH) is a ubiquitous intracellular peptide with diverse functions that include detoxification, antioxidant defense, maintenance of thiol status, and modulation of cell proliferation. Dysregulation of GSH synthesis is increasingly being recognized as contributing to the pathogenesis of many pathological conditions. These include diabetes mellitus, pulmonary fibrosis, cholestatic liver injury, endotoxemia and drug-resistant tumor cells. Manipulation of the GSH synthetic capacity is an important target in the treatment of many of these disorders. PMID: 18601945
- The results of this study indicate that the use of GSH is a safe new method for high-dose cisplatin administration. This regimen is well-tolerated and very effective in ovarian cancer patients with bulky disease and warrants further evaluation. PMID: 2306797
- These findings suggest that mild iron deficiency and low GSH levels, which are associated with increased oxidative stress, increase the risk of oral cavity cancer. PMID: 18584481
- These findings suggest that GSH is able to attenuate the nephrotoxicity induced by CDDP, not only when administered prior to CDDP (Cisplatin, cis-diamminedichloroplatinum), but also when administered at the same time as or subsequent to CDDP administration, without affecting the anticancer activity of CDDP. Thus, the administration of GSH is a promising approach for attenuating the nephrotoxicity caused by CDDP. PMID: 22895541
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