LIPID-PEROXIDATION AND ANTIOXIDANT ENZYME-ACTIVITIES IN THE RAT TESTIS AFTER CIGARETTE-SMOKE INHALATION OR ADMINISTRATION OF POLYCHLORINATED-BIPHENYLS OR POLYCHLORINATED NAPHTHALENES

Lipid peroxidation products and antioxidant enzyme activities were stu died in the rat testis following exposures to cigarette smoke, polychl orinated biphenyls (PCBs), or polychlorinated naphthalenes (PCNs). Thr ee hours after a single 1-hour period of smoke inhalation, the levels of fluorescent chromolipids and thiobarbituric acid-reactive species ( TBARS) were markedly increased in the testis (+49%, P < 0.01, and +43% , P < 0.05, respectively). Twelve hours after daily smoking for 1 hour , for 1, 5, or 10 days, such an increase was not found. Activities of the antioxidant enzymes superoxide dismutase (SOD), catalase, glutathi one peroxidase (GSH-Px), glutathione transferase (GSH-Tr), or hexose m onophosphate shunt (HMS) were not affected immediately, 3 hours, or 12 hours after a single smoking session. Twelve hours after smoking for 5 days, the activity of catalase was decreased (-16%, P < 0.05). Smoki ng exposures had no consistent effects on serum follicle-stimulating h ormone (FSH), luteinizing hormone (LH), or testosterone concentrations . Single i.p. injections of PCB or PCN mixtures resulted in decreases in testicular SOD activity 1 day after the exposures (-14%, P < 0.05, and -51%, P < 0.01,respectively). Catalase activity also decreased aft er both exposures (-30 to -42%, P < 0.05, at days 1-7 after PCB exposu re, and -37 to -43%, P < 0.05, at days 3-7 after PCN exposure). Ninety days after the PCN exposure, activities of GSH-Px and GSH-Tr were dec reased in the testis (-20%, P < 0.05, and -26%, P < 0.05, respectively ). The only statistically significant change in lipid peroxidation mea surements in the testes of PCB- or PCN-treated rats was a decrease in TBARS by 13% (P < 0.01) 1 day after PCN exposure. The main findings of this study were the increase in lipid peroxidation in the rat testis after cigarette smoke inhalation and the impairment of the function of the enzymatic antioxidant defense after exposures to PCBs or PCNs. Th ese results suggest that free radical-dependent mechanisms may play an important role in the testicular toxicity of environmental chemicals.