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NADH donates an electron at Complex I, generating NAD + , while FADH 2 donates two electrons at Complex II, generating FAD

Histologically, it consists of anastomosing capillary-like vessels with a loosely lobular architecture

[16] [18] Animal studies have not demonstrated teratogenicity, but high doses in pregnancy may theoretically increase the risk of fetal oxalate nephropathy or other metabolic disturbances

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Studies with genetically encoded sensors for Ca 2+ cycling and SV exocytosis revealed the core roles of mitochondria in presynaptic Ca 2+ clearance [54, 55]