Occupational exposure and experimental intoxication with acrylamide (ACR) produce a neuropathy characterized by nerve degeneration. We hypothesize that ACR differentially affects the expression of bcl-2, bax and caspase-3 in the central nervous system (CNS) and the peripheral nervous system (PNS) tissue. Male adult Wistar rats were given ACR (20, 40 mg/kg i.p. 3 days/week) for 8 weeks. Samples of the cerebral cortex, cerebellum, spinal cord and sciatic nerves were collected and examined for bcl-2, bax and caspase-3 expression using Western blotting. Subchronic exposure to ACR reduced cortical bcl-2 expression in the low dose, increased it in the high dose; the change of bcl-2 expression in the spinal cord and cerebellum followed the same pattern as that described in the cerebral cortex; there was no significant change in the expression of bax in the cerebral cortex and the spinal cord, however, in the cerebellum the change of bax expression and bcl-2 expression is just the reverse. Thus, the bcl-2/bax ratio of the CNS tissue was affected by exposure to ACR, it decreased in the low dose group and increased in the high group. Compared to control, densitometric analysis showed that in the sciatic nerves the expression of bcl-2 and bax expression was markedly increased following ACR administration. The expression of inactive isoforms (32 kDa) of caspase-3 was not altered in the cortices of ACR-treated rats, but increased in their spinal cords and sciatic nerves. Thus, subchronic exposure to ACR affected the expression of death-related proteins in the CNS and PNS tissue, which indicate there is the early molecular regulatory mechanism of apoptosis in the neuropathy induced by ACR.