The objective of this study was to analyse male sexual behaviour under hypoglycemia and to examine the patho-physiology of free radical presence. Animals (Rattus norvigecus) were divided into control and streptozotocin (STZ) treated groups. At the end of 120 days, mating behavior study and libido and potency measurements were made and the pituitary gonadal axis was analyzed by radio-immuno assay. Tissues were harvested after sacrificing animals by overdose of anesthesia intraperitoneally. (thiopentone sodium 40mg/kg of body wt.). Enzymic, non enzymic antioxidant, HO., and H2O2 were estimated. Brain tissues were fixed in 10 % formalin for histological analyses, apoptosis of MOPA neurons were measured by TUNNEL method and monoamine detection by the Glioxylic acid method. Tyrosine hydroxylase (TH), D2 receptor expression and synaptophysin of MPOA were studied. Mating behavior showed a significant increased in mounting and intermission latency (Diabetes vs. Control) (11.16 ± 0.16 vs. 38.51 ± 0.13 and 10.14 ± 0.13 vs. 25.45 ± 1.38 seconds (s)), ejaculation latency (253.83 ± 2.98 vs. 1040.65 ± 36.84. s) and post ejaculatory interval (474.08 ± 5.44 vs. 1150.48 ± 52.28. s), decrease in number of intromission, number of mount and inter intromission interval (17.92 ± 0.23 vs. 32.25 ± 8.05. S) in the hypoglycemic rats. Test of potency showed significant reduction in erection (p< 0.001), quick flip (p< 0.001), long flip (p< 0.01) and total genital reflex (p< 0.001). Compared to control, diabetic animals showed significant reduction in enzymatic (SOD – p< 0.001) CAT – p< 0.001 GPx – p<0.01, GST – p<0.001), non enzymatic antioxidants level (Vit-C – p< 0.001, Vit-E – p< 0.001, GSH – p< 0.05) and significant increase in amount of LPO (p < 0.001), HO. (p< 0.01) and  H2O2 (p<0.001) was found in the hypothalamus of STZ treated rats. Apoptosis in MPOA neurons was increased in the hypoglycemic animals. TH enzyme activity, monoamine and synaptophysin levels were significantly reduced in STZ rats when compared with control. Increased exposure of MPOA to ROS might have reduced monoamine biosynthesis or increased auto-oxidation or might altered the D2 receptor expression in MOPA, leading to male sexual behavior impairment. High ROS could reduce synaptic terminals by increased neuronal degeneration in MPOA or derangement of pituitary testicular axis may contribute to sexual behavior disorder viz. Reduced population of androgen dependent neurons. Present observation of male sexual disorder in animal model may form a useful insight into human sexual behavioral disorder under oxidative stress.