THE EFFECT OF DEVELOPMENTAL EXPOSURE TO CADMIUM (CD) ON VISUAL-EVOKEDPOTENTIALS (VEP) AND LIPID-PEROXIDATION

Pregnant Swiss albino rats were divided into three groups: control (C) , gestational exposure of Cd (G-Cd), and gestational/postnatal exposur e of Cd (GP-Cd) groups. Control animals received tap water, and the ra ts of GP-Cd group received Cd as CdCl2 in their drinking water during the experimental period. The G-Cd group was given Cd during pregnancy, but given tap water after birth. Twenty-two days after birth, 15 rats (for each group) were taken from their mothers and continued to be tr eated with Cd (GP-Cd group) or tap water (C and G-Cd groups) for an ad ditional 38 days. On postnatal day (PND) 60, flash visual evoked poten tials (FVEPs) were recorded with disc electrodes attached with collodi on 0.5 cm in front of and behind bregma. The mean latencies on N1, P2, and P3 were prolonged in the GP-Cd group compared with controls. The mean latency of P3 was also significantly different between G-Cd and G P-Cd groups. P1-N1 and N1-P2 amplitudes of VEPs were significantly dec reased in the GP-Cd group compared with control group. N1-P2 amplitude of the G-Cd group was significantly lower than that of the control gr oup. Thiobarbituric acid reactive substances (TBARS) were determined a s an indicator of lipid peroxidation. Our data showed that pre- and po stnatal Cd treatment caused a significant increase of lipid peroxidati on in the brain. (C) 1997 Elsevier Science Inc.