The diagnosis of congenital methemoglobinemia is based on the level of the intracellular cytochrome b5
Due to deficiency of enzyme nicotinamide adenine dinucleotide NADH cytochrome b5
reductase, which helps in conversion of methaemoglobin to functional haemoglobin.
Recent studies have shown that the hybrid parenchymal cells of the ZF and ZR co-express 3[sz]-hydroxysteroid dehydrogenase (3[sz]HSD) and cytochrome b5
(Cyt-b5), affecting the production of androstenedione., Moreover, Cyt-b5 enhances the activity of 3[sz]HSD by reinforcing the affinity of 3[sz]HSD and its cofactor nicotinamide adenine dinucleotide NAD(+).
vannamei FE103086.1 - Electron transport chain complex III Cytochrome b5
P450 oxidoreductase (POR) and cytochrome b5
are also important for 17-OH/17,20-lyase enzyme activity.
In both [Ogg1.sup.-/-] and [Ogg1.sup.+/+] PB-treated mice livers, comparable significant overexpression of CAR and PXR downstream enzymes involved in xenobiotic metabolism including CYP2B10, CYP3A11, CYP2A5, CYP1A2, CYP2C54, cytochrome b5
type A (CYB5A), carboxylesterase 1 (CES1), POR, GST alpha 3 (GSTA3) and alpha 4 (GSTA4), GST mu 1 (GSTM1), GST mu 3 (GSTM3), GST mu 5 (GSTM5), UDP-glucose 6-dehydrogenase (UGDH), and paraoxonase 1 (PON1) was demonstrated by proteome analysis.
However, the activities of cytochrome b5
(CB) and N.N dimethyl aniline N-oxide (DAO) decreased 76% and 38%, respectively.
This is not uncommon since the [V.sub.max] value is a function of the expression level of enzyme, which varies from one study to another based on enzyme concentration, incubation conditions, different ratios of co-enzymes (NADPH-CYP reductase or cytochrome b5
) versus CYP1A2 in incubation mixtures, and different phospholipid composition between liver microsomes and the recombinant enzyme system.
When SARA was induced, acyl-CoA synthetase (ACS) and cytochrome b5
involved in lipid metabolism were up-regulated, phosphoenolpyruvate carboxykinase (PEPCK) involved in glucose metabolism was downregulated, while enolase was up-regulated.
We also report the in silico docking of theaflavin with cytochrome b5
reductase which is the constituent of PMRS.
Congenital or inherited causes of methemoglobinemia result due to decreased activity of the enzyme cytochrome b5
reductase resulting in diminished enzymatic reduction of the hemoglobin molecule.
The transformation of this iron to ferric iron ([Fe.sup.+3]) by losing electron is prevented by cytochrome b5
system of the body and normally only 1-2% of hemoglobin is present in ferric state in the body.