Elleh, B.I*1, Thompson, I. N.2 1Department of Chemical Pathology, Federal University Otuoke, Bayelsa State, Nigeria 2Department of Chemical Pathology, Rivers State University, Port Harcourt, Nigeria   *Corresponding author: Elleh B.I.  Abstract The aim of this study was to evaluate oxidative stress biomarkers and antioxidant status in rabbits following topical application of herbal cosmetics. Three herbal oils were named sample A, B, C and a total of 48 rabbits grouped into four were used for the study. Rabbits from each group were treated for thirty, sixty and ninety days respectively with 0.5ml/kg of Samples A, B, C and distilled water as control. At days thirty, sixty and ninety, respectively, four rabbits from each group were sacrificed under chloroform anesthesia. Blood samples were collected for investigation of biochemical parameters at intervals of, 30days, 60days and 90days respectively. GraphPad Prism version 7.0 was used for statistical analysis and pThe results of malondialdehyde (MDA), Total Antioxidant Capacity (TAC), Lipid Peroxidation Index (LPI) and C-Reactive Index (CRP) at day 30 and 60 in sample A, B and C showed no significant difference compared to control. However, at day 90 the mean values of MDA, LPI, TAC and CRP were statistically significant p. The results showed that heavy metals present in the cosmetics can induce oxidative stress by stimulating reactive oxygen species production, enhancing lipid peroxidation and depleting antioxidant reserves. Therefore, the resulting oxidative damage may contribute to the pathogenesis of chronic diseases, including cardiovascular disease. Keywords: Oxidative Stress, Biomarkers, Antioxidant Status and Rabbits Introduction The use of cosmetics is a common practice particularly among women. However, concerns have been raised regarding the presence of heavy metals as contaminants in several cosmetic products. Heavy metals such as lead (Pb), cadmium (Cd), mercury (Hg), arsenic (As) and chromium (Cr) have been detected in skin-lightening creams, lipsticks, eye liners and facial powders at concentrations that sometimes exceed regulatory limits [1], [2]. Chronic dermal exposure to these products represents a potential route of systemic metal absorption, with implications for oxidative stress and associated health outcomes. Oxidative stress occurs as a result of an imbalance between the production of reactive oxygen species and the ability of biological systems to detoxify these reactive intermediates or repair the resulting damage. Heavy metals induce oxidative stress through multiple mechanisms. Although some metals like Pb and Cd are not redox-active, they deplete antioxidant reserves by binding to sulfhydryl groups of glutathione and antioxidant enzymes such as superoxide dismutase, catalase and glutathione peroxidase [3]. Other metals such as Hg and Cr can participate in Fenton-like reactions, leading to the generation of highly reactive hydroxyl radicals. The resultant increase in reactive oxygen species causes lipid peroxidation, protein oxidation and DNA damage [4]. Several studies have reported elevated biomarkers of oxidative stress in individuals exposed to heavy metals through cosmetic use. [5] analyzed facial cosmetics sold in Nigeria and found Pb, Cd and Hg levels above WHO permissible limits. The authors suggested that prolonged dermal application could lead to systemic accumulation and subsequent oxidative tissue injury. Similarly, [6] reported significant levels of Pb and Cd in lipsticks and eye pencils marketed in Nigeria, highlighting the potential for chronic low-dose exposure. Experimental and occupational studies provide further mechanistic evidence. Cadmium exposure has been shown to increase malondialdehyde, a marker of lipid peroxidation, while decreasing superoxide dismutase, catalase and glutathione activities in liver and kidney tissues [7]. Lead toxicity is associated with increased reactive oxygen species generation and depletion of antioxidant enzymes, resulting in hepatocellular damage [8]. Exposure to heavy metals is strongly associated with increased oxidative stress in humans. Heavy metals such as lead (Pb), cadmium (Cd), mercury (Hg) and arsenic (As) are redox-active or indirectly generate reactive oxygen species through depletion of antioxidant defenses. Once absorbed through dermal, inhalation or ingestion routes, these metals accumulate in target organs including the liver, kidney and vascular endothelium, where they disrupt cellular redox balance [4]. Several studies have consistently reported elevated levels of oxidative biomarkers in individuals with chronic heavy metal exposure, suggesting a key mechanistic link between metal toxicity and tissue damage. The primary pathway involves the induction of oxidative stress and lipid peroxidation. Lead and cadmium, for example, do not directly participate in Fenton reactions but they inhibit antioxidant enzymes and bind to