Pharmacological and biochemical studies on the role of free radicals during stress-induced immunomodulation in rats.

The present study was designed to evaluate the role of free radicals in restraint stress (RS)-induced modulation of immune responses in rats. RS significantly suppressed both humoral and cell-mediated immune responses as evidenced by reduced (a) anti-SRBC antibody titre (b) splenic Plaque Forming Cell counts, (c) footpad thickness response, and (d) IFN-γ and IL-4 levels. Assay for oxidative stress markers in blood showed that there was significant enhancement in plasma corticosterone and products of lipid peroxidation, viz. malondialdehyde and lowered reduced glutathione levels on exposure to RS. Further, this was associated with decreased antioxidant enzyme activity, viz. superoxide dismutase and catalase. These RS-induced changes in immunological and oxidative stress markers were markedly attenuated by pretreatment with the antioxidants, L-ascorbic acid (100 and 200 mg/kg) and α-tocopherol (30 and 60 mg/kg), by differential degrees. The combination of L-ascorbic acid and α-tocopherol was shown to have synergistic effects on reversal of these RS-induced effects. The results suggest that reactive oxygen species may be involved in stress-induced immunomodulation.