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10.1074/jbc.M212633200 106

Theories on the biochemistry of these end-organ changes include toxic effects from sorbitol accumulation, vascular damage by excessive glycosylation with crosslinking of basement membrane proteins, and activation of protein kinase C-2 by vascular endothelial growth factor (VEGF), leading to increased vascular permeability and endothelial cell proliferation

Patients with hepatic impairment : No dosage adjustment is required

Neurotoxicant-induced animal models of Parkinsons disease: understanding the role of rotenone, maneb and paraquat in neurodegeneration

Epigallocatechin-3-gallate potently inhibits the in vitro activity of hydroxy-3-methyl-glutaryl-CoA reductase