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Hypothetical Molecular Mechanisms Underlying Hyperhomocysteinemia-Mediated Vascular Disorders Hyperhomocysteinemia-Mediated Oxidant Stress through Imbalanced Thiol Redox Status Numerous studies indicate that oxidant stress plays a role in the development of occlusive atherosclerotic lesions that are observed primarily in homozygotes for the CBS defect (McCully, 1983) and later in experimental hyperhomocysteinemia

This prevents bacterial growth and allows for multiple withdrawals from the same vial over time

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