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& Gabreels, F

& Cherezov, V

2.1.2.1 Effects of AP on hepatic oxidative stress The oxidative stress and inflammation have long been proposed as an important biochemical mechanism underlying the development of liver injury (Jaeschke, 2000)

These include aquaglyceroporin (AQP), formate-lactate channel (FNT), putative copper channel, cationic amino acid transporter (NTP1), hexose transporter (HT1), putative amino acid transporter (AAT1, AAAP3), putative Mg 2+ transporter, ATP: ADP antiporter (AAC1, AAC2), putative MCP1, folatebiopterin transporter (FT1, FT2), equilibrative nucleoside transporter (ENT, ENT4), Zn 2+ and Fe 2+ transporter (ZIPCO), the ABC transporters known as multidrug-resistant proteins (MDR1, MDR2, and MDR5) and multidrug-resistant associated proteins (MRP1 and MRP2), putative inorganic anion exchanger (SulP), Pi: Na + symporter (PiT), putative lipid/sterol: H + antiporter (NPC1R), V type H + ATPase, and a variety of P-ATPases (ATP1, ATP2, ATP4, ATP8, CuTP, and GCa)

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A provider should assess your baseline B12 and micronutrient status to ensure both therapies align with your metabolic needs and tolerability profile