Bisphenol A (BPA) is a controversial chemical. The possible toxic effect of BPA on the function of the heart has not been studied in detail till to date. So, the aim of the present study was to examine the effect of BPA on the ventricular function of heart at the molecular physiological level in rat. Studies were performed on adult male rats of Sprague- Dawley strain (150-200gm, n=7). BPA was administered at a dose of 50mg/kg body weight/day for 20 and 30 days by oral gavage. The rats were sacrificed by cervical dislocation on the 24th hour after the last treatment. Paraffin embedded ventricular tissue sections were stained with hematoxylin and eosin (H&E); and Von-Kossa’s technique after Bancroft et al, 2008. The activities of superoxide dismutase (SOD)(Marklund and Marklund,1974), catalase (CAT)(Sinha,1972), glutathione reductase (GR)(Staal et al,1969), glutathione peroxidase (GPX)(Rotruck et al, 1973) were determined and the amount of malondialdehyde (MDA)(Devasagayam and Tarachand,1987) was estimated in microsomal fraction of ventricular myocytes (VMs). Acetylcholinesterase (AChE) activity was measured after Ellman et al,1961. Values are means±S.E.M., compared by Student’s t-test. We found significant changes in the size and shape of the nucleus of VMs in H&E stained tissue sections of test rats in a duration dependent manner. Moreover, many lacunae were seen in the matrix of the VMs. We also observed significant deposition of Ca2+-salt at all durations in Von-Kossa’s stained ventricular tissue section. These findings suggest that BPA damages the VMs and hampers calcium homeostasis by causing Ca2+-salt deposition in VMs. The activities of antioxidant enzymes were seen to be decreased in both 20 and 30 days durations compared to the control groups [(SOD-6.51±0.2 vs. 7.08±0.3 and 6.47±0.2 vs. 6.58±0.3 U/mg protein)(CAT-25.18±0.4 vs. 27.06±0.5 and 24.42±0.5 vs. 26.59±0.6 U/mg protein, p<0.05)(GPX-3.61±0.3 vs. 4.78±0.3 and 3.77±0.2 vs. 4.87±0.4 nmoleGSH/mg protein, p<0.05)(GR-16.23±0.6 vs. 24.28±0.9 and 11.48±0.5 vs. 23.94±0.8 nmoleNADPH oxidized/min/mg protein, p<0.001) respectively]. While, the MDA production was increased in test groups than control groups in both durations [(16.66±0.5 vs. 14.96±0.5 and 19.74±0.2 vs. 13.98±0.7 nmole MDA/mg protein-p<0.001) respectively]. These results suggest that BPA induces oxidative stress in rat VMs by depleting antioxidant defense system and increasing lipid peroxidation. Further, the activity of AChE was decreased significantly in treated rats in both durations [(4.43±0.4 vs. 10.19±0.6 and 3.91±0.3 vs. 10.19±0.6 μmole/min/mg protein, p<0.001) respectively]. This suggests that BPA inhibits ventricular functions by inhibiting AChE at the ventricular synapse. In conclusion, BPA inhibits ventricular function in rat presumably by hampering Ca2+-homeostasis and causing oxidative stress in VMs; and inhibiting AChE activity in ventricular synapse.