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The primary aim of this study is to elucidate the molecular mechanisms underlying CP-induced ovarian injury, with a focus on oxidative stress, inflammatory signaling, and apoptotic pathways, focusing on nuclear factor-kappa B (NF-B), nuclear factor erythroid-2-related factor 2/heme oxygenase-1 (Nrf2/HO-1), Toll-like receptor 4 (TLR4), nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, silent information regulator-1 (SIRT1), and other signaling pathways involved in the pathogenesis of ovarian injury caused by CP

However, at a constant concentration of GSH with varying concentrations of GSH, Lineweaver-Burk and Hofstee plots of initial velocity as function of glutathione concentration revealed apparent K m and Vm values: 27.62 M and 0.66 nmoles ml -1 min -1 respectively

2003;284:H60512

doi: 10.1186/s13073-020-00796-5 127 ChenMLTakedaKSundrudMS