Elaidic acid enhanced the simultaneous neurotoxicity attributable to the cerebral pathological lesion resulted from oxidative damages induced by acrylamide and benzo(a)pyrene

Acrylamide (ACR), benzopyrene [B(a)P] and trans-fatty acids (TFA) could be found to co-exist in many foods processed by high temperature. Our study investigated the effects of elaidic acid (ELA), a predominant TFA, on neuropathology induced by simultaneous exposure of ACR and B(a) P to mice. Results showed ELA enhanced the decrease of weight gains induced by simultaneous exposure of ACR and B(a) P (AB). Moreover, ELA enhanced ACR-induced increase of gait abnormality, B(a) P-induced damage to learning and memory, and AB-induced both of the damage above. Meanwhile, ELA enhanced B(a) P-induced axonal degeneration in hippocamp, ACR- and AB-induced up-regulating of abnormal cerebellar Purkinje cells. ELA enhanced ACR-induced up-regulating of MDA in cerebrum and 8-OHdG in cerebrum and cerebellum; ELA enhanced B(a) P-induced up-regulating of MDA in cerebrum, PCO in cerebellum and 8-OHdG in cerebrum and cerebellum. Meanwhile, the enhancing role of ELA, on ACR-induced reduction of SOD activity in cerebrum and cerebellum, on B(a) P-induced reduction of GPx activity in cerebrum were found. Results suggested that ELA play a enhancing role on ACR-induced and B(a) P-induced oxidative damage, which attributable to the cerebral pathological lesion, and subsequent effect on gait abnormality and deficit on learning and memory in mice.