Strawberry fruit (Fragaria x ananassa Romina) juice attenuates oxidative imbalance with concomitant modulation of metabolic indices linked to male infertility in testicular oxidative injury.

Abstract

This study investigated the protective properties of strawberry fruit on testicular oxidative injury. Oxidative injury was induced in vitro in testicular tissue homogenates by incubation with ferrous sulphate (FeSO4 ) in the presence and absence of strawberry fruit extract (SFE) for 30min at 37˚C, with gallic acid serving as the standard antioxidant drug. Induction of oxidative injury significantly reduced glutathione, cholesterol and triglyceride levels; and inhibited SOD, catalase and ENTPDase activities when compared to normal control. It also led to exacerbated nitric oxide, malondialdehyde, LDL-cholesterol levels, acetylcholinesterase, ATPase and lipase activities. These effects were, however, reversed following treatment with SFE when compared to the untreated control, except for cholesterol and triglyceride levels. Additionally, the induction of the oxidative injury led to alterations in testicular lipid metabolites that were accompanied by the activation of α-linolenic acid and linoleic acid metabolic pathways. While SFE treatment had no significant impact on the altered metabolites, it repressed pathways for mitochondrial beta-oxidation of long-chain saturated fatty acids and plasmalogen synthesis. High-performance liquid chromatography analysis of SFE revealed the presence of rutin, caffeic acid, p-coumarin and cinnamic acid. These data imply the protective potentials of strawberry fruits against testicular oxidative injury.