The hypothesis was tested that the magainin pcptides. known to compromise bacterial and mitochondrial energetic& are highly active against spermatozoa. A mixture of magainin A and PGLa (l:I) caused a SO% rcdsction in mc :i!ity of hamster spermatozoa at 4 @ml total pcptide concentration, All motility was lost at 8 .~g/ml. At this concentration, respiratory control was released and respiration in the presence of uncoupler was inhibited. Uptake of the lipophilic cation tetraphcnyl phosphonium was largely abolished by addition of magainin A and PGLa at this concentration, indicative of a decrease in the mitochondridl membrane potential. Magainin A and PGLa showed synergism with respect to release of respiratory control.

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Tumor necrosis factor alpha (TNF alpha), a pleiotrophic cytokine present in atherosclerotic lesions, caused a dose-dependent and persistent reduction in gap junctional intercellular communication (GJIC) between primary human smooth muscle cells in vitro. A continuous presence of TNF alpha was required for this persistent inhibition. Pretreatment of smooth muscle cells with ascorbic acid, alpha-tocopherol or glutathione prevented this inhibition of GJIC by TNF alpha. The persistent blockage of GJIC by continuous exposure to TNF alpha suggests that TNF alpha may share some mechanistic similarities with exogenous tumor promoters. Furthermore, this reduction in GJIC by TNF alpha may provide an additional link between the processes of atherosclerosis and carcinogenesis. The protection afforded by antioxidant compounds suggests a role for active oxygen species in the promotion stage of atherosclerosis.

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