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Glucose-6-phosphate dehydrogenase is not essential for K-Ras-driven tumor growth or metastasis

Mechanistically, SLC25A39 overexpression maintains mitochondrial function, while its deficiency disrupts mitochondrial protein import and complex I activity, resulting in excessive ROS generation, loss of mitochondrial membrane potential, DNA damage, ATP depletion, and impaired electron transport, ultimately triggering apoptosis

Role of Nrf2/HO-1 Signal axis in the Mechanisms for Oxidative Stress-Relevant Diseases

Homocysteine levels can be high for a number of reasons:[ref][ref] Insufficient folate and B12 (exacerbated by variants in MTHFR, MTR see genotype report below) Not enough B6 (CBS pathway, B6 see genotype report) More methionine than the body can handle Renal insufficiency (kidney disease) or alcoholism Genetic mutations in the CBS gene can cause rare cases of hyperhomocysteinemia