Studies on biochemical mechanism of neurotoxicity induced by acrylamide in rats

The effects of acrylamide on calmodulin (CaM), cAMP, cGMP, Ca2+, Mg(2+)-ATPase and 45Ca2+ uptake in nervous system were determined in Wistar rats (ip, 10 or 50 mg.kg-1 for 12 d). The results indicate that acrylamide caused an alteration in calcium homeostasis in rat brain by decreasing the Ca(2+)-sequestering capacity of microsomes, and this may occur due to an efflux of calcium secondary to a microsomal structure damage. The changes of CaM in nervous system coupled with potential alteration in the intracellular Ca2+ concentration could affect many CaM-dependent enzymes (i.e. Ca2+, Mg(2+)-ATPase) and cyclic AMP system, and CaM or cAMP is known to be "toxicological second messenger" that could initiate neurotoxicity, though more work is needed to elucidate the details of the mechanism.