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Elevated iron in the SNpc, reduced glutathione, and widespread oxidation of lipids document the oxidative milieu in post-mortem PD brains, whereas deficits in complex I activity and impaired mitophagy underscore the pivotal role of dysfunctional mitochondria in reactive oxygen species (ROS) overload
The main sinusoidal transport system for bile-salt uptake is the Na+-taurocholate cotransporting polypeptide, which has been cloned from both rat (Ntcp, Slc10a1)50 and human liver (NTCP, SLC10A1).51 Ntcp/NTCP is driven by a transmembrane Na+ gradient maintained by the Na+/K+-ATPase pump, which is also strategically localized in the sinusoidal membrane.52 Ntcp/NTCP accounts for the transport of more than 80% of amidated bile salts (the major circulating bile salts), and only 40% of their unconjugated, parent compounds.53 The remaining fraction of circulating bile salts is taken up by a non-electrogenic, Na+-independent transport system, formed by a family of transporters collectively named organic aniontransporting polypeptides (Oatps/OATPs for rat and human, respectively).54 Humans possess four OATPs: OATP1A2 (SLCO1A2/SLC21A3), OATP1B1 (SLC21A6), OATP1B3 (SLC21A8) and OATP2B1 (SLC21A9)
They significantly impact the majority of vitamin D-related effects and are recognized for modulating approximately 3% of the human genome [4, 17]
