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When infection and inflammation persist, however, mitophagy and a selective autophagy with ferritin serving as a substrate are simultaneously activated, and they increase free iron levels released from cells and mediate an uncontrolled cascade reaction, leading to the death of many immune cells and sepsis-induced immunosuppression (Table 1) [208, 209]
Craig: Totally
In cells, homocysteine is metabolized in three ways :[ref] It can be remethylated to form methionine (requires folate, MTHFR, and vitamin B12, MTR gene or needs betaine, interacting with BHMT and PEMT genes) Can be converted to cysteine (CBS gene, serine and B6 as a cofactor), which is used in the synthesis of glutathione It can be converted to homocysteine thiolactone, which can be a problem at higher levels Lets dig into each of these pathways further: Methylation Cycle: Homocysteine, Methionine, SAMe, and SAH Homocysteine is maintained at a relatively constant level by several mechanisms in the methionine cycle
Two B-complex vitamins, folic acid and Vitamin B12, essential for red blood cell formation in bone marrow
