The effect of pre and postnatal cadmium exposure on somatosensory evoked potentials: relation to lipid peroxidation

Pregnant swiss albino rats were divided into three groups: control (C), gestational exposure of cadmium (G-Cd) and gestational/postnatal exposure of cadmium (GP-Cd) groups. Control animals received tap water and the rats of GP-Cd group received Cd as CdCl2 in their drinking water during the experimental period. 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 treated with Cd (GP-Cd group) or tap water (C and G-Cd groups) for an additional 38 days. On postnatal day (PND) 60, somatosensory evoked potentials (SEPS) of three groups were recorded following left posterior tibial nerve (PTN) stimulation. The mean latencies of N1, P1, and N2, components were significantly prolonged in both Cd groups compared with control group. The mean latency of N1 in the GP-Cd group was longer than control and the G-Cd groups. There was no significant amplitude differences among groups. On the other hand, thiobarbituric acid reactive substances (TBARS), an indicator of lipid peroxidation, were increased in the sciatic nerves of both groups compared with control group. A significant increase in the TBARS level of the brain was found only in GP-Cd group due to significant accumulation of Cd.