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Evidence from multiple fields, including metabolism, cell biology, and clinical endocrinology, collectively suggests that within the uterine fibroid microenvironment, E 2 and progesterone may induce excessive ROS accumulation through three pathways: enzyme metabolic imbalance, mitochondrial dysfunction, and disruption of the antioxidant system

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Characterization of the serotoninergic system in the C57BL/6 mouse skin

These specialized enzymes transfer electrons from cytoplasmic NADPH to generate ROS that initiate lipid peroxidation

Activity of herpes simplex virus type 1 latency-associated transcript (LAT) promoter in neuron-derived cells: evidence for neuron specificity and for a large LAT transcript