γ-aminobutyric acid (GABA) inhibits programmed cell death in fresh-cut pumpkin by maintaining mitochondria structural and functional integrity

Abstract

The beneficial effects of γ-aminobutyric acid (GABA) on oxidative damage and programmed cell death (PCD) in fresh-cut pumpkins were preliminarily demonstrated in our previous research. However, the mechanism by which GABA alleviates PCD in fresh-cut pumpkins remains unclear. In this study, we discovered that GABA treatment effectively reduced mitochondrial structural damage and membrane permeability while increasing the mitochondrial membrane potential (ΔΨm) in fresh-cut pumpkins compared to the control. Additionally, GABA-treated pumpkins exhibited higher adenosine triphosphate (ATP) content and energy charge, consistent with increased activity of H+-ATPase, succinate dehydrogenase (SDH), malate dehydrogenase (MDH), and cytochrome c oxidase (COX). Conversely, the activity of alternative oxidase (AOX), Ca2+-ATPase, and K+-ATPase was reduced in GABA-treated pumpkins compared to the control. Moreover, key factors in apoptosis, such as the activity of six caspases and the gene expression of apoptosis-inducing factors (CmAIFs) and metacaspases (CmMCAs), were significantly decreased following GABA treatment. In conclusion, GABA effectively suppressed PCD in postharvest fresh-cut pumpkins by improving mitochondrial physiological properties and energy metabolism while inhibiting apoptosis-related factors.