Incidence of environmental lead contamination and its effects on the health of humans and animals are increasing globally. Previous studies have shown that experimental lead exposure predisposes the stomach to gastric ulceration (Olaleye et al, 2006). However, there is paucity of information on how chronic lead exposure will interfere with processes leading to gastric ulcer healing. In this study, the effects of chronic lead exposure on gastric mucosal antioxidant status and epithelial cell apoptosis during ulcer healing in rats were investigated. Sixty rats (80-100g) were randomly divided equally into control (tap water), low and high dose (Lead acetate, 100 ppm and 5,000 ppm respectively, p.o.) groups. Twenty weeks post-treatment, ulcers were induced in the stomachs of the animals by serosal application of 60% acetic acid after anesthesia (thiopental sodium: 50mg/Kg) (Wang et al, 1989). The level of SOD activity was determined by the method of Misra and Fridovich (1972). The method of Hunter et al., (1963), modified by Gutteridge and Wilkins (1980), was used for MDA assay. Apoptosis was determined by Terminal deoxynucleotidyl-transferase-mediated dUTP Nick-End Labeling (TUNEL) assay. Values are means ± S.E.M., compared by ANOVA and Student’s t-test at P<0.05. Lead treatment increased ulcer areas for low (10.0±0.4mm square, 8.0±0.4 mm square and 2.9± 0.1mm square) and high (14.4±0.2 mm square , 10.5±0.3 mm square and 3.9± 0.3mm square) dose groups on days 7, 14 and 21 respectively compared to control (7.9± 0.12, 4.82 ± 0.14 and 1.46 ± 0.17mm square on days 7, 14 and 21 respectively). For MDA activity, on day 0, the values were 4.9±0.11, 5.8±0.18 and 6.7±0.35 µmol MDA/g of wet tissue. During healing, MDA activities in all groups on day 7 were 12.5±0.28, 13.2 ±0.32 and 40.5 ± 0.61µmol MDA/g of wet tissue (for control, low dose and high dose respectively). By day 21, the values were 5.4±0.21, 7.9± 0.32 and 20.5±0.32 µmol MDA/g of wet tissue for control, low dose and high dose groups. For SOD activity, the values (on day 0), were 1.5±0.02, 1.9±0.04 and 2.0±0.05 µg/mg protein for control, low dose and high dose respectively (p<0.05). However, during healing, there were no significant differences in SOD activities in both experimental groups compared to control. Lead (high dose) increased epithelial cell apoptosis (25.3±4.88, 23.8±2.02 and 19.3±3.57 apoptotic cells/unit area compared to control values of 3.9±1.55, 9.8±0.86 and 2.8±0.75 apoptotic cells/unit area) on days 7, 14 and 21 respectively. In conclusion, chronic exposure of rats to lead delayed gastric ulcer healing via increased gastric lipid peroxidation (as measured by MDA levels) and increased epithelial cell apoptosis while there were no significant changes in SOD levels.