The objective of current study was to evaluate the neuroprotective effects of bacoside A and bromelain against dichlorvos induced toxicity. The healthy, 6-8 weeks old male Swiss mice were administered in separate groups subacute doses of dichlorvos (40 mg/kg bw), bacoside A (5 mg/kg bw) and bromelain (70 mg/kg bw). In order to determination of oxidative stress in different groups, thiobarbituric acid reactive substances (TBARS) and protein carbonyl content (PCC) were studied in the present investigation. Moreover, for toxic manifestation at molecular level the site-specific gene amplification of acetylcholinesterase (AChE) gene was studied in the brain. Nonetheless, the protective effects of bacoside A and bromelain were also evaluated on the TBARS, PCC and AChE gene. The exposure of dichlorvos leads to significant increase in TBARS level (p < 0.01, p < 0.001) and PCC. Besides, the decline in DNA yield, expression of amplified products of AChE gene was observed in the brain of dichlorvos treated group. The bacoside A and bromelain treatments significantly decreased the level of TBARS (p < 0.05, (p < 0.01) and PCC whereas, increase in the DNA yield and expression of amplified AChE gene products were observed in the brain compared to only dichlorvos treated mice. The overall picture which emerged after critical evaluation of results indicated that the dichlorvos induced oxidative stress and alteration in AChE gene expression showed significant improvement owing to the treatments of bacoside A and bromelain. Thus, bacoside A and bromelain are very effective in alleviating neurotoxicity induced by dichlorvos.