1997
DOI: 10.1006/taap.1997.8151
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Potent Protective Effect of Melatonin on Chromium(VI)-Induced DNA Single-Strand Breaks, Cytotoxicity, and Lipid Peroxidation in Primary Cultures of Rat Hepatocytes

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Cited by 115 publications
(70 citation statements)
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“…The present study also showed that chromium (VI) treatment resulted in decreased levels of nonenzymatic antioxidants such as GSH, vitamins C and E, and inhibited activities of enzymatic antioxidants such as GR, GSH-Px and SOD in cultured rat hepatocytes. Similar results were observed in previous studies [40][41][42]. In the present study, pretreatment with DDTC had no effect on the reduction of GSH or vitamin C level or on inhibition of GR, GSH-Px or SOD activity induced by chromium (VI).…”
Section: Discussionsupporting
confidence: 93%
See 1 more Smart Citation
“…The present study also showed that chromium (VI) treatment resulted in decreased levels of nonenzymatic antioxidants such as GSH, vitamins C and E, and inhibited activities of enzymatic antioxidants such as GR, GSH-Px and SOD in cultured rat hepatocytes. Similar results were observed in previous studies [40][41][42]. In the present study, pretreatment with DDTC had no effect on the reduction of GSH or vitamin C level or on inhibition of GR, GSH-Px or SOD activity induced by chromium (VI).…”
Section: Discussionsupporting
confidence: 93%
“…Concerning these antioxidants, our previous studies with cultured hepatocytes also showed that a metal chelator DFO had no influence on cellular levels of GSH and the activities of GR as well as SOD, however this chelator attenuated the suppression of cellular levels of vitamin C and vitamin E induced by chromium (VI), resulting in the suppression of chromium (VI)-induced DNA breaks, cytotoxicity and lipid peroxidation [41]. Similarly, treatment with vitamin E or melatonin inhibited chromium (VI)-induced cytotoxicity as well as lipid peroxidation, and normalized the levels of vitamins C and E suppressed by dichromate, without affecting such antioxidant enzymes as GSH-Px, SOD and CAT [40,42]. These and the present study suggest that the protective effect of DDTC against chromium (VI)-induced cytotoxicity and lipid peroxidation may be related more to the levels of nonenzymatic antioxidants such as vitamin E than to the enzymatic antioxidant activity within cells.…”
Section: Discussionmentioning
confidence: 99%
“…All these findings indicate that AFMK is a central metabolite of melatonin oxidation especially in nonhepatic tissues. Interestingly, melatonin was shown to prevent the loss of important dietary antioxidants including Vitamins C and E (Susa et al 1997), bind iron and participate in maintaining iron pool at appropriate level resulting in control of iron haemostasis, thereby providing tissue protection (Othman et al 2008). Furthermore, melatonin enhances antioxidant action of atocopherol and ascorbate against NADPH-and iron-dependent lipid peroxidation in human placental mitochondria (Milczarek et al 2010).…”
Section: Melatonin and Factors That Determine Antioxidant Capacitymentioning
confidence: 99%
“…72 Experimentally, melatonin has been shown to cause some restoration in vitamin C and E levels (nonenzymatic antioxidants) and the activity of catalase (an enzymatic antioxidant) in cells exposed to oxidative stress. 73 In vitro studies show that melatonin scavenges a common oxidantFnitric oxide. 74 It also protects against chromosomal damage caused by ionizing radiation and other oxidative stresses.…”
Section: Melatonin and The Lensmentioning
confidence: 99%
“…74 It also protects against chromosomal damage caused by ionizing radiation and other oxidative stresses. 73 Whereas most antioxidants can only function within certain subcellular compartments, its lipid 35 and aqueous 36 solubility allow access to virtually all parts of the cell.…”
Section: Melatonin and The Lensmentioning
confidence: 99%