The aim of this work was to determine if the inhibition or stimulation of NO synthesis modulates liver damage induced by chronic lead intoxication. Lead nitrate (3.6 mg/kg, per os) was administered one time a day for 30 days to male Wistar rats with low and high resistance to hypoxia treated simultaneously with L-arginine (600 mg/kg, i.p.) or N^ω-nitro-L-arginine (L-NNA, 35 mg/kg, i.p.) 30 min. before lead exposure. L-Arginine treatment protected the liver of rats with low resistance to hypoxia partially by reducing lipid hydroperoxides level, the thiobarbituric acid reactive substances (TBARS) concentration, and altering the antioxidant defense system depletion induced by lead intoxication. Treatment of lead-exposed highly resistant rats by L-arginine did not reduce the TBARS level, but lowered the lipid hydroperoxides concentration. The increased glutathione antioxidant defense system in liver of L-NNA-treated rats reflects the antioxidant action of L-NNA for this animal group.