Abstract:
Dietary exposure to cadmium, even at lower doses, can lead to free radical induced neurotoxicity,
neurobehavioral changes and alteration in neurotransmitters. Such changes are likely to
be more pronounced in the developing brain due to incompleteness of blood brain barrier
(BBB). Hippocampus being the seat of intelligence has a role in learning and cognitive behavior
and any damage to hippocampus during developmental stage is likely to result in neurodegenerative
changes in later life. To this end, fetal and neonatal exposure to cadmium was induced
by exposing pregnant dams of Swiss albino strain throughout the period of gestation
and following parturition up till 5th day post partum (pp) through drinking water
(3ppm/animal/day). The neonates were sacrificed on day 6 pp and indices of oxidative stress,
levels of trace elements and changes in cholinergic system were evaluated in the hippocampus.
Increased lipid peroxidation, surge in reactive oxygen species (ROS), depressed antioxidant
defense, increased accumulation of cadmium, differential alterations in trace elements
and decreased activity of AChE were the features of cadmium toxicity. Simultaneous administration
of melatonin to cadmium challenged animals offset these detrimental changes. The
results suggest that melatonin co-administration can effectively protect against the adverse
effects of cadmium on endogenous antioxidant status, changes in trace metal concentrations
and compromised hippocampal cholinergic system.
