ABSTRACT:The antioxidant activity of the aqueous crude extract of Ocimum gratissimum Linn. leaf on the basal and traumatized (cadmium-induced) serum levels of alkaline phosphatase (ALP), total acid phosphatase (ACP T ) and prostatic acid phosphatase (ACP P ) of the male guinea-pig (GP) were evaluated. Preliminary experimentation showed that the effects of the aqueous crude extract of O. gratissimum on basal serum phosphatases were slightly more in the oral than the intraperitoneal (i.p) route. Oral administration of 20mg of O. gratissimum caused a timedependent decrease in the basal serum levels of ACP T and ACP P without an effect on ALP values. The inhibitory effects compared to the control were maximum at 4 hours. Furthermore, O. gratissimum given orally, caused significant dose-dependent decreases (p<0.05) of the basal serum levels of ACP T and ACP P at p<0.05. Basal serum concentrations of ACP T and ACP P changed from 23.50±1.04 and 7.50±0.29 to 8.25±0.75 and 2.25±0.29 IU at 20mg, representing 65 and 70 % decreases respectively. In contrast, 0.25-8mg/kg of cadmium (Cd) given intraperitoneally, caused significant dose-dependent increases (p<0.05) in the phosphatase enzymes. However pretreatment with 5mg of the crude extract, which on its own had little effect on basal serum phosphatase levels, followed by i.p administration of Cd, caused a reversal of the Cd-induced dose-response curves on the various phosphatase levels to negative values. These results may be due to the oxidative and the antioxidative biochemical antagonistic properties of the agents used in these experiments. They may also be due to enzyme conformational changes and effects of eugenols and flavonoids in the crude extract of O. gratissimum. @ JASEM Oxidation is an essential process in all organisms which involves redox reactions. These reactions normally generate reactive oxygen species (ROS) or highly reactive free radicals that can react virtually with all cell components to cause tissue injury (Collier et al., 1992). Exogenous sources of free radicals include tobacco smoke, ionization radiation, certain pollutants such as cadmium, vanadium, crude oil, organic solvents and pesticides (Robinson et al., 1997). The resulting oxidative free radicals are obligate intermediates of many metabolic reactions but may also cause pathological damage (Floyd et al., 1990). Similarly, antioxidation is the reversal of the above described processes mediated through scavenging of the free radicals, by dismutase enzyme systems, and phenolic-rich compounds such as flavonoids (Sardesai 1995;Rice-Evans et al., 1996). The body has evolved a number of interrelated antioxidant mechanisms to maintain redox homeostasis (Toyokuni et al., 1999). These antioxidant mechanisms include antioxidant enzymes: superoxide dismutase (SOD), catalase (CAT), gluthathione peroxidase (GSH-Px), heme oygenase (HO) etc (Ames et al., 1993;Sardesai 1995;Sies, 1997;Vertuani et al., 2004). A disturbance in the balance between the production of reactive oxygen species or free radicals an...