Protective effect of deferoxamine on chromium(VI)-induced DNA single-strand breaks, cytotoxicity, and lipid peroxidation in primary cultures of rat hepatocytes |
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Authors: | Nobuyuki Susa Shunji Ueno Yoshinori Furukawa Masayasu Sugiyama |
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Institution: | (1) Department of Veterinary Public Health, School of Veterinary Medicine and Animal Sciences, Kitasato University, Towada, Aomori 034, Japan, JP;(2) Asunaro Pharmacy, 6–7 Hatsune-cho, Tobataku, Kitakyushu 804, Japan, JP |
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Abstract: | Incubation of primary cultures of rat hepatocytes with K2Cr2O7 and deferoxamine (DFO), an iron chelator, resulted in a marked decrease in cellular levels of DNA single-strand breaks caused
by K2Cr2O7. Cellular treatment with DFO also suppressed both dichromate-induced cytotoxicity – evaluated by the leakage of lactate dehydrogenase,
and lipid peroxidation – as monitored by malondialdehyde formation. In addition, treatment with DFO attenuated the suppression
of the levels of vitamin E and C as well as the inhibition of alkaline phosphatase and glutathione peroxidase activity attributed
to K2Cr2O7. However, DFO had no influence on the cellular level of glutathione or the activity of glutathione reductase and superoxide
dismutase suppressed by dichromate. Under the same experimental conditions, cellular uptake and distribution of chromium were
not affected by DFO. These results indicate that DFO protects cells from chromium(VI)-induced DNA strand breaks, cytotoxicity,
lipid peroxidation, vitamin E and C depression, and glutathione peroxidase inhibition. The role of antioxidants in chromium(VI)-induced
cytotoxicity, DNA breaks, and lipid peroxidation is discussed.
Received: 17 September 1996 / Accepted: 25 November 1996 |
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Keywords: | Chromium(VI) Deferoxamine DNA breaks Cytotoxicity Lipid peroxidation |
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