The dead and damaged spermatozoa present in the fresh ejaculates are carried passively along with the live ones into the processed semen. Such dead and damaged spermatozoa are primarily responsible for the production of reactive oxygen species (ROS). The detrimental effect by way of oxidative stress on the contemporary live spermatozoa results in poor fertility (Roca, Martinez-Alborcia, Gil, Parrilla, & Martinez, 2013). Since the buffalo spermatozoa show high lipid peroxidation (LPO) rate (Nair, Brar, Ahuja, Sangha, & Chaudhary, 2006), comparatively reduced activity of existing antioxidant system (Nair et al., 2006), high content of membrane polyunsaturated fatty acids (Dawra, Sharma, & Makkar, 1983) and increased susceptibility to osmotic stress the damage owing to oxidative stress is exaggerated (Kadirvel, Kumar, & Kumaresan, 2009). The nuclear integrity as well as plasma membrane fluidity is also affected by LPO is another consequence of concern (Roca et al., 2013). In live spermatozoa, production of free radicals is of mitochondrial origin, mostly for the physiological processes. However, the imbalance of free radicals arise either due to excessive production intracellularly under physiological situations