The impact of Triton WR-1339 induced hyperlipidemia on the effects of benzo(a)pyrene or guaiacol on α- and γ-tocopherol pools and selected markers of pro-/antioxidative balance in rat plasma and erythrocytes.

The toxicity of carcinogenic benzo(a)pyrene (BaP) can be intensified by the pro-oxidative effects of metabolic activation. The oxidatively active products can be formed during enzymatic biotransformation or in the process of co-oxygenation with lipid peroxidation. This study assesses if the acute hyperlipidemia can increase pro-oxidative effects of BaP as a factor intensifying processes of lipid peroxidation and co-oxygenation. After three days of i.p. administration of BaP or guaiacol (equimolar dose 10mg/kg b.w.) without or with the hyperlipidemia inducer-Triton WR-1339 to male Wistar rats, the levels of α- and γ-tocopherol were measured in erythrocytes and plasma together with the level of lipid peroxidation as malonyldialdehyde (MDA) concentration. Guaiacol was chosen as a reference substance due to its high ability to co-oxygenate. Additionally, the activity of superoxide dismutase (Cu,ZnSOD) in erythrocytes and plasma was monitored. In normolipaemic groups the significant decrease in erythrocyte α-tocopherol pool and the increase in lipid peroxidation level were observed after BaP or guaiacol administration. In hyperlipaemic groups, despite the increase in the level of lipid peroxidation, there were no additional effects in tocopherol pools compared to the normolipaemic groups which could be attributed to co-oxygenation. Decrease of α-tocopherol in erythrocytes was proportional to the reduction in normolipemic subjects when accounting for the migration to hyperlipemic plasma. There was no co-oxygenation effect on the activity of superoxide dismutase (Cu,ZnSOD) in blood.