Estrogen protects females against cardiovascular diseases in both receptor-dependent, genomic or non-genomic manner. Although part of the protective effects is attributed to its enhancement of nitric oxide (NO) production and antioxidant properties, in vivo evidence is difficult to establish. We thus employed paraquat (PQ)-treated rats as a model for oxidative stress and to compare oxidative damage determined by malondialdehyde (MDA) contents as index for lipid peroxidation of various tissues. Samples from aorta, lung, and liver exhibited low but detectable MDA level in intact control rats; sham operation did not but PQ-treatment significantly enhanced the MDA levels of all tissues. Different hormonal status were achieved by comparing sham-operated (sham), sham treated with estrogen receptor antagonist ICI182,780 (ICI), and ovariectomized (OVX) rats. OVX significantly reduced plasma estrogen level, ICI effectively blocked estrous cycle without reducing estrogen level. Derived from rats subjected to identical PQ treatment, MDA level was significantly higher in OVX rats than that of sham in isolated aortic rings. In lung tissues, MDA level were similar in all groups. In liver tissues, ICI rats exhibited higher level of MDA than both sham and OVX rats. These data indicated that hormonal status could affect the degree of lipid peroxidation under similar oxidative stress induced by PQ, and that not all tissues responded identically.