Abstract

The present study attemps to define the capacity of methylprednisolone sodium succinate (MP) to protect neuronal membranes against a free radical challenge in primary cultures of fetal mouse spinal cord. Incubation of these cultures with MP significantly increased the Na +,K +-ATPase activity, an effect that was blocked by the RNA synthesis inhibitor, actinomyosin D and the protein synthesis inhibitor, cycloheximide, suggesting an induction of protein synthesis by MP. In contrast, incubation with FeCl 2 for 1 or 2 h significantly inhibited Na +,K +-ATPase activity and elevated the levels of thiobarbituric acid-reactive substances (TBARS). Pretreatment with MP prevented the rise in TBARS and partially prevented the decrease in Na +,K +-ATPase activity for the first hour of FeCl 2 incubation, an effect that was lost during the second hour. A second dose of MP after the first hour of incubation with FeCl 2 partially restored Na +,K +-ATPase activity and reduced TBARS levels after the second hour of exposure to FeCl 2. Co-incubation of MP with cycloheximide completely prevented the decrease in Na +,K +-ATPase activity seen after a 2-h incubation with FeCl 2 and eliminated the need for a second dose of MP after the first hour of incubation with FeCl 2. These findings suggest a capacity for rapid protein induction and antioxidant activity for MP in vitro.

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