Lysine and Tryptophan have the Protection Basis against Lysosomal Dysfunction and both PKU and CVD including Mitochondrial Disorder Mediated by Activating Lysosomes and OPA1

Abstract

The phenylketonuria “PKU” due to sever decreasing in lysine “AAG” and in Lys/ phosphorylation (which necessary for lysosomal digestive function), and associated with sever decreasing in Trp “TGG”, followed by mitochondrial dysfunction and lysosomal dysfunction, that followed by sever decreasing in phe /hydroxylase and in Tyr/ hydroxylase, and followed by decreasing in lysine acylation and in SFACs productiin which followed by decreasing in RA productive pathway and associated with increasing in both of TNFa and cholesterol accumulation which activate increasing in in both of TNFa and NLRP3 pathogenic pathway which reflect decreasing in estrogen synthesis and in dopamine production, that followed by increasing in the risk of ischemic damage pulmonary disease and diabetes.
And we can conclude that both of Lys “AAG” and Trp “TGG” are so necessary for activating mitochondrial oxidative functions and necessary for promoting transport system where Mitochondria is so necessary to activate antioxidant function and promoting all of Phe hydroxylase, Tyr hydroxylase, and Lys acylation production which necessary for dopamine and RA synthesis respectively, where the PKU characterized by sever decreasing in antioxidant function, and sever decreasing in both Phe/ hydroxylase & Trp/ hydroxylase production, followed by decreasing in dopamine production and decreasing in retinoic acid production (which due to the reduction in SFACs synthesis).And I concluded that PKU characterized by sever decreasing in Phe /hydroxylase and Tyr /hydroxylase, followed by reduction in dopamine production, and reduction in alpha amylase, that associated with increasing in TNFa and in NLRP3 pathogenic pathway, and associated with increasing in the pulmonary disease and CVD risk.Retionic acid “RA”  is regulated by lysine  acylation and is regulated by lysine acylation mediated by short fatty acid synthesis, which regulate aminoacyl-tRNAs production regulated by mitochondrial enzymes and regulate mRNA production by E coli (regulated by phenylalanine) that necessary to run antioxidant functions and cellular biosynthesis.The antihypertensive pathway mechanism is: the Lysine →activate ATPase and both lysosomes and Mitochondrial oxidative functions which activate lysine acylation →activate short fatty acid synthesis →stimulate retinoic acid “RA” synthesis - →where both Lys and Trp activate GTPase which promote  mitochondria repair and oxidative functions, which activate, Phe/ hydroxylase, and activate Tyr/ hydroxylase which activate dopamine, followed by activating NR4As pathway which responsible for activating GC-beta and both of Oxytocin and Nrf2, followed by Ang2-AT2 and VEGF-A productive functions and heme oxygenase production (notice dopamine regulate heme oxygenase mediated by dopamine beta-hydroxylase which regulated by Mitochondrial oxidative functions) followed by activating anti-inflammatory growth and processes.
Lysine Methylation has important role to enhance and adopt hypertension through activating RA and pervious Antihypertensive pathway mediated by Phe/hydroxylase synthesis and Tyr /hydroxylase production followed by activating both of dopamine and NR4As pathway.