The article discusses the importance of the glutathione-ascorbic acid antioxidant system in animals, focusing on the role of glutathione (GSH) and ascorbic acid (vitamin C) in protecting cells from reactive oxygen species (ROS). GSH, a tripeptide, is crucial for protecting against oxygen toxicity and is synthesized in most animal cells. Depletion of GSH, often induced by administering a transition-state inhibitor like L-buthionine-(SR)-sulfoximine (BSO), leads to severe cellular damage and multiorgan failure in newborn rats and guinea pigs, highlighting the critical role of GSH in cellular survival. Ascorbate, which can be recycled from dehydroascorbate, plays a significant role in preventing GSH deficiency and its associated damage. Studies in adult mice, which can synthesize ascorbate, show that while GSH deficiency still causes tissue damage, ascorbate can mitigate these effects. In guinea pigs, ascorbate deficiency leads to scurvy, but treatment with GSH ester can delay the onset of symptoms. The interplay between GSH and ascorbate is complex, involving both enzymatic and nonenzymatic reactions, and further research is needed to fully understand their roles in maintaining cellular health and protecting against oxidative stress.The article discusses the importance of the glutathione-ascorbic acid antioxidant system in animals, focusing on the role of glutathione (GSH) and ascorbic acid (vitamin C) in protecting cells from reactive oxygen species (ROS). GSH, a tripeptide, is crucial for protecting against oxygen toxicity and is synthesized in most animal cells. Depletion of GSH, often induced by administering a transition-state inhibitor like L-buthionine-(SR)-sulfoximine (BSO), leads to severe cellular damage and multiorgan failure in newborn rats and guinea pigs, highlighting the critical role of GSH in cellular survival. Ascorbate, which can be recycled from dehydroascorbate, plays a significant role in preventing GSH deficiency and its associated damage. Studies in adult mice, which can synthesize ascorbate, show that while GSH deficiency still causes tissue damage, ascorbate can mitigate these effects. In guinea pigs, ascorbate deficiency leads to scurvy, but treatment with GSH ester can delay the onset of symptoms. The interplay between GSH and ascorbate is complex, involving both enzymatic and nonenzymatic reactions, and further research is needed to fully understand their roles in maintaining cellular health and protecting against oxidative stress.