Susa N, Ueno S, Furukawa Y, Sugiyama M
Department of Veterinary Public Health, School of Veterinary Medicine and Animals Sciences, Kitasato University, Aomori Japan.
Arch Toxicol. 1997;71(6):345-50. doi: 10.1007/s002040050397.
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.
用重铬酸钾（K2Cr2O7）和铁螯合剂去铁胺（DFO）处理大鼠肝细胞原代培养物，可使由K2Cr2O7引起的细胞DNA单链断裂水平显著降低。用DFO进行细胞处理还可抑制重铬酸盐诱导的细胞毒性（通过乳酸脱氢酶泄漏评估）和脂质过氧化（通过丙二醛形成监测）。此外，用DFO处理可减轻因K2Cr2O7导致的维生素E和C水平的降低以及碱性磷酸酶和谷胱甘肽过氧化物酶活性的抑制。然而，DFO对谷胱甘肽的细胞水平或被重铬酸盐抑制的谷胱甘肽还原酶和超氧化物歧化酶的活性没有影响。在相同实验条件下，DFO不影响细胞对铬的摄取和分布。这些结果表明，DFO可保护细胞免受六价铬诱导的DNA链断裂、细胞毒性、脂质过氧化、维生素E和C降低以及谷胱甘肽过氧化物酶抑制。讨论了抗氧化剂在六价铬诱导的细胞毒性、DNA断裂和脂质过氧化中的作用。
