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In light of these intracellular observations (Kokame et al, 1996), we hypothesize that changes in the intracellular redox state associated with elevated homocysteine levels can alter the expression of multiple genes involved in other specific cellular functions that could be partially responsible for vascular disorders associated with moderate hyperhomocysteinemia

3.2.1 Steroidogenic enzyme inhibition 3.2.1.1 17-hydroxysteroid dehydrogenase (HSD17B) suppression Cadmium exposure directly inhibits HSD17B enzymatic activity with an IC50 of 2.2 M, resulting in an 85% reduction in testosterone synthesis capacity

Group 4 didn't receive any treatment [36]

Don't inject it until the discrepancy is resolved