DEHP impairs the oxidative stress response and disrupts trace element and mineral metabolism within the mitochondria of detoxification organs.

This article focuses on the effects of di(2-ethylhexyl) phthalate (DEHP), a widely used plasticizer and endocrine-disrupting chemical, on mitochondrial function in the liver and kidneys of rats. The study demonstrates that DEHP exposure impairs mitochondrial antioxidant enzyme activities (including glucose 6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, glutathione reductase, glutathione S-transferase, and glutathione peroxidase), disrupts essential trace element and mineral homeostasis (notably sodium, magnesium, copper, zinc, and iron), and alters key oxidative stress-related signaling pathways such as NF-κB, Akt, STAT3, and CREB in these detoxification organs. These findings provide novel insights into the mitochondrial mechanisms underlying DEHP toxicity, highlighting mitochondria as critical targets contributing to oxidative damage and metabolic dysregulation in detoxification organs. The study underscores the importance of further research on DEHP's impact on human and environmental health.