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The disruption mechanisms of oxidative stress include oxidative damage to cellular components (protein oxidation, lipid peroxidation, and DNA damage), activation of matrix metalloproteinases, cytoskeleton reorganization, modulation of tight junction proteins, and upregulation of inflammatory mediators [81, 86, 87]
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The clinical evidence for these drugs is robust and their safety profiles are well-established
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[9] Concomitant administration of large calcium supplements, thiazide diuretics, or aluminium-containing phosphate binders can potentiate vitamin D-mediated increases in serum calcium or phosphate, demanding periodic laboratory monitoring and dosage adjustments to avert nephrolithiasis or ectopic calcification
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