LEAD is the most common cause of poisoning in cattle and young calves are highly susceptible. This heavy metal has also been incriminated as a cumulative environmental poison having no beneficial biological role. The toxic effects of pollutant ranges from overt clinical signs refer- able to nervous, gastrointestinal and haemopoietic systems to subclinical subtle effects (Swarup 1996). Various mech- anisms have been put forth to explain the lead-induced pathotoxicity such as interaction of lead with bioactive lig- ands resulting in inactivation of several vital enzyme sys- tems, disturbances in mineral metabolism and demyelination of nervous tissue (Valle and Ulmer 1972, Klassen 1985). However, the suggested mechanisms have not been fully defined. Recent studies in vitro and in labo- ratory animals and occupationally exposed workers sug- gest that at least some lead-induced damage may occur as a consequence of the propensity of lead to disturb the deli- cate prooxidant and antioxidant balance that exists in mammalian cells (Lima-Hermes et al 1991, Donaldson and Knowles 1993, and Monteiro et al 1985). However, there is no literature relating to oxidant and antioxidant status and thiol groups on livestock exposed to lead. The objectives of the present study were to determine the effect of oral expo- sure to lead for a period of 28 days on erythrocyte antioxi- dant enzyme activities, thiol groups and lipid peroxide level. MATERIALS AND METHODS Animals and experimental design The experiment was conducted on 20 healthy male calves, aged between 25 to 35 days. They were fed whole milk during early age and subsequently with whole milk plus calf starter and green fodder. Calves were randomly divided into two groups, group A (N = 5) and group B (N = 15). Calves of group B were given 0·75 per cent aque- ous solution of lead acetate at the rate of 1 ml kg –1 body weight (=7·5 mg of lead acetate or 4·097 mg lead kg –1 body weight orally for a period of 28 days whereas those of group A received no treatment and served as unexposed healthy control. Blood samples were collected from jugular vein from all experimental animals on day 0, and thereafter at weekly intervals (day 7, 14, 21 and 28) during the period of lead exposure. Chemicals Tris cacodylic acid, diethylenetriamine pentaacetic acid (DTPA), Nitroblue tetrazolium, pyrogallol and thiobarbi- turic acid were purchased from Sigma Chemicals, USA. Nitric acid, NaH 2 PO 4 2H 2 O, KH 2 PO 4 , Lead acetate 99 per cent pure, Excelar grade from BDH, India. 5–5¢ Dithiobis 2 nitro benzoic acid extrapure from Sisco Research laborato- ries, India. Analysis of metals Approximately 5 ml blood sample was collected in nitric acid washed heparinized vials and was wet digested with nitric acid and perchloric acid mixture (Kolmer et al 1951). Lead concentration in the blood samples was estimated using Effect of lead on erythrocytic antioxidant defence, lipid peroxide level and thiol groups in calves R. C. PATRA, D. SWARUP Division of Medicine, Indian Veterinary Research Institute, Izatnagar – 243122 (U.P.), India SUMMARY Fifteen crossbred male calves were exposed to lead for a period of 28 days orally at the dose rate of 7·5 mg of lead acetate as 0·75 per cent solution kg –1 body weight to study its effect on erythrocytic antioxidant defense, lipid peroxide level and thiol groups. Five calves were given no treatment and served as unexposed controls. Blood samples were collected before exposure to lead and there- after at weekly intervals (ie. on day 7, 14, 21 and 28). Erythrocyte haemolysate (10 per cent) was prepared and analysed for lipid per- oxide level, activity of Superoxide dismutase (SOD) and catalase. Total, protein-bound and non protein-bound thiol groups were also measured. Exposure to lead significantly (P < 0·05) reduced the erythrocytic SOD activity by day 7 and it remained lower until day 21 followed by a marginal increase on day 28. Catalase activity declined after an initial compensatory rise on day 7. Erythrocytic lipid peroxide level was recorded to be significantly (P < 0·05) higher by day 21 and 28 of exposure. Total, protein-bound and non protein- bound -SH content of erythrocytes declined. It was concluded that oral exposure of lead reduced the erythrocytic thiol content and antioxidant defence indicating possible role of free radicals in pathogenesis of lead toxicity. © 2000 Harcourt Publishers Limited 0034-5288/00/010071 + 04 $35.00/0 © 2000 Harcourt Publishers Ltd *Corresponding author: R. C. Patra, Division of Medicine, IVRI, Izatnagar – 243122 (U.P.), India Research in Veterinary Science 2000, 68, 71–74 doi:10.1053/rvsc.1999.0340, available online at http://www.idealibrary.com on