Melatonin stimulates brain glutathione peroxidase activity

Barlow‐Walden, Lornell; Reíter, Russel J.; Abe, Mitsushi; Pablos, Marta I.; Menéndez-Peláez, Armando; Chen, L. D.; Pöeggeler, Burkhard

doi:10.1016/0197-0186(94)00154-m

Cited by 501 publications

(285 citation statements)

References 25 publications

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“…However, aMT mainly reduces NO• through the inhibition of its synthesizing enzyme, nitric oxide synthase NOS (Escames et al, 2003). In addition to these scavenging action, aMT also stimulates several antioxidative enzymes including SOD, and glutathione peroxidase (GPx) and reductase (GPx); these actions further reduce the oxidation state in the majority of cells (Antolin et al, 1996;Barlow-Walden et al, 1995;Okatani et al, 2000;Pablos, 1997).…”

Section: Introductionmentioning

confidence: 99%

Improved mitochondrial function and increased life span after chronic melatonin treatment in senescent prone mice

Rodríguez

Escames

López

et al. 2008

Experimental Gerontology

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Section: Introductionmentioning

confidence: 99%

Improved mitochondrial function and increased life span after chronic melatonin treatment in senescent prone mice

Rodríguez

Escames

López

et al. 2008

Experimental Gerontology

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“…One major function of melatonin is to scavenge radicals formed in oxygen metabolism, thereby potentially protecting against free radical induced damage to DNA, proteins and membranes [190][191][192][193] . It has been shown that melatonin stimulates the antioxidative enzyme GPx in the brain, thus providing indirect protection against free radical attack 194) . In animal experiments, melatonin prevented the induction of free radical damage caused by a variety of conditions including ingestion of toxins, ionizing radiation, ischemia, reperfusion and excessive exercise 192,[195][196][197][198] .…”

Section: Melatoninmentioning

confidence: 99%

Strategies for Safe and Effective Therapeutic Measures for Chronic Arsenic and Lead Poisoning

Kalia¹,

Flora²

2005

Journal of Occupational Health

266

161

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Strategies for Safe and Effective Therapeutic Measures for Arsenic and LeadPoisoning: Kiran Kalia, et al. Department of Biosciences, Sardar Patel University, IndiaExposure to toxic metals remains a widespread occupational and environmental problem in world. There have been a number of reports in the recent past suggesting an incidence of childhood lead poisoning and chronic arsenic poisoning due to contaminated drinking water in many areas of West Bengal in India and Bangladesh has become a national calamity. Low level metal exposure in humans is caused by air, food and water intake. Lead and arsenic generally interferes with a number of body functions such as the central nervous system (CNS), the haematopoietic system, liver and kidneys. Over the past few decades there has been growing awareness and concern that the toxic biochemical and functional effects are occurring at a lower level of metal exposure than those that produce overt clinical and pathological signs and symptoms. Despite many years of research, we are still far from an effective treatment of chronic plumbism and arsenicosis. Medical treatment of acute and chronic lead and arsenic toxicity is furnished by chelating agents. Chelating agents are organic compounds capable of linking together metal ions to form complex ring-like structures called chelates. They have been used clinically as antidotes for acute and chronic poisoning. 2, 3-dimercaprol (BAL) has long been the mainstay of chelation therapy for lead or arsenic poisoning. Meso 2, 3, -dimercaptosuccinic acid (DMSA) has been tried successfully in animals as well as in a few cases of human lead and arsenic poisoning. DMSA could be a safe and effective method for treating lead or arsenic poisoning, but one of the major disadvantages of chelation with DMSA has been its Review inability to remove lead from the intracellular sites because of its lipophobic nature. Further, it does not provide protection in terms of clinical/ biochemical recovery. A new trend in chelation therapy is to use combined treatment. This includes the use of structurally different chelators or a combination of an adjuvant and a chelator to provide better clinical/ biochemical recovery in addition to lead mobilization. The present review article attempts to provide update information about the current strategies being adopted for a safe, effective and specific treatment for two major toxic metals or metalloid.

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“…It also acts as an indirect antioxidant through the activation of major antioxidant enzymes including SOD, CAT, and GPx (36)(37). Improved liver function after melatonin treatment seems to be a consequence of this effect.…”

Section: Discussionmentioning

confidence: 99%

Melatonin Improves Liver Function in Benzene-Treated Rats

Sharma

Rana

2013

Archives of Industrial Hygiene and Toxicology

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In this study, we investigated the benefi cial effects of melatonin against benzene-induced liver function impairments in Wistar rats. After 30 days of treatment, it signifi cantly lowered hepatosomatic indices, bilirubin, and hydroxyproline in male and female benzene-treated rats. Even though it did not infl uence aspartate aminotransferase, melatonin had benefi cial effects on alanine aminotransferase and alkaline phosphatase. Our results suggest that melatonin is an effective modulator of liver function in benzenetreated rats thanks to its antioxidative properties.

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Melatonin stimulates brain glutathione peroxidase activity

Cited by 501 publications

References 25 publications

Improved mitochondrial function and increased life span after chronic melatonin treatment in senescent prone mice

Improved mitochondrial function and increased life span after chronic melatonin treatment in senescent prone mice

Strategies for Safe and Effective Therapeutic Measures for Chronic Arsenic and Lead Poisoning

Melatonin Improves Liver Function in Benzene-Treated Rats

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