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  • Title: Vitamin E protection from/potentiation of the cytogenetic toxicity of cisplatin in Swiss mice.
    Author: Choudhury RC, Jagdale MB.
    Journal: J Chemother; 2002 Aug; 14(4):397-405. PubMed ID: 12420859.
    Abstract:
    Possible protection from or potentiation of the cytogenetic toxic effects of cisplatin (CP) 5 mg/kg b.w. in mouse bone marrow, spermatogonia by three different doses of alpha-tocopheryl acetate (vitamin E) 100, 200 and 300 mg/kg, and the transmission of such effects in the male germline, were assessed. CP-induced chromosomal aberrations (CAs) in bone marrow were decreased in vitamin E pretreated mice, but significantly (P < or = 0.05) only with vitamin E 300 mg/kg. The percentages of dividing cells in bone marrow were increased in vitamin E-pretreated groups of mice, but not significantly. However, the frequency of CP-induced micronuclei (MN) in polychromatic erythrocytes (PCEs) declined significantly (P < or = 0.01) in all the vitamin E-pretreated groups of mice. In spermatogonia the CP-induced CAs were also decreased significantly by vitamin E 200 mg/kg (P < or = 0.01), and 100 and 300 mg/kg (P < or = 0.05). However, transmission of CP-induced cytogenetic toxic effects from spermatogonia to spermatocyte, resulting in the formation of aberrant primary spermatocytes, was enhanced significantly in the mice pretreated with vitamin E 100 mg/kg (P < or = 0.05) and 200 mg/kg (P < or = 0.01). But the enhancement in the transmission of such effects was not significant in the mice pretreated with vitamin E 300 mg/kg. Besides, there was no significant change in vitamin E-pretreated groups of mice in the transmission of cytogenetic toxicity of CP from spermatogonia to sperm with the manifestation of abnormal sperm morphology. Thus, vitamin E protected bone marrow and spermatogonia from the cytogenetic toxic effects of CP, particularly efficiently at the highest tested dose (300 mg/kg), but it failed to protect from the transmission of such effects in the male germline of mouse and rather potentiated them to some extent. Treatment with vitamin E, an antioxidant, might be capable of protecting noncancerous cells from the oxidative damage caused by cisplatin but it might also reduce the effects of cisplatin on cancerous cells. Thus, the benefits of antioxidant treatment during cancer chemotherapy is yet to be demonstrated clearly.
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