S. Sarkar et al., LIPID PEROXIDATIVE DAMAGE ON CADMIUM EXPOSURE AND ALTERATIONS IN ANTIOXIDANT SYSTEM IN RAT ERYTHROCYTES - A STUDY WITH RELATION TO TIME, BioMetals, 11(2), 1998, pp. 153-157
Cadmium induced lipid peroxidation (LPO) and the activity of antioxida
nt enzymes after the administration of a single dose of CdCl2 (0.4 mg
kg(-1) body wt, ip) was studied in rat erythrocytes. Cd intoxication i
ncreased erythrocyte LPO along with a decrease in superoxide dismutase
(SOD) up to three days of Cd treatment. The decrease in erythrocyte c
atalase (CAT) activity was marked within 9 h of Cd intoxication. After
three days of Cd treatment, LPO decreased towards normal, along with
an increase in erythrocyte SOC and CAT activity. Blood glutathione (GS
H) decreased significantly within 24 h of Cd treatment, followed by an
increase towards normal. Erythrocyte glutathione S-transferase (GST)
activity increased up to 10 days of Cd intoxication, probably in an at
tempt to reduce Cd toxicity. Serum glutamate pyruvate transaminase (SG
PT), serum alkaline phosphatase (SALP) and serum bilirubin increased u
p to 10 days of Cd intoxication. Blood urea increased significantly up
to three days, followed by a decrease towards normal. The results sho
w that Cd induced LPO was associated with a decrease in antioxidant en
zymes and GSH in erythrocytes; as these antioxidants increase in eryth
rocytes with recovery from Cd intoxication, the Cd induced LPO reverse
d towards normal. The increase in the SGPT, SALP and serum bilirubin c
orrelated with LPO. The results suggest that Cd intoxication induces o
xidative stress and alters the antioxidant system, resulting in oxidat
ive damage to rat erythrocytes.