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Since GSH is the final product of the homocysteine metabolism in the transsulfuration pathway by transferring sulfur from homocysteine to cysteine, a deficiency in transsulfuration pathway leads to excessive homocysteine production (hyperhomocysteinemia) and reduced GSH synthesis (159, 160)
Furthermore, pristine SiO 2 NPs, which could not be taken up by erythrocytes, were shown to promote ROS-mediated and caspase-3-dependent eryptosis [452] (Fig
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We investigated serum levels of homocysteine, aminotransferases, fasting blood glucose (FBG), lipids, malondialdehyde (MDA), and homeostasis model assessment of insulin resistance (HOMA-IR)
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