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Magnesium Research

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Mechanisms of cataractogenesis in the presence of magnesium deficiency Volume 26, numéro 1, January-February-March 2013

Auteurs
Universiti Teknologi MARA, Faculty of Medicine, Level 20, Tower 1, Science & Technology Complex, 40450 Shah Alam, Selangor, Malaysia, Volgograd State Medical University, Department of Pharmacology, 1 Pavshikh Bortsov sq., 400131 Volgograd, Russian Federation, International Medical University, IMU Clinical School, Department of Ophthalmology, Jalan Rasah, Seremban, Negeri Sembilan, Malaysia

Senile cataract is the most common cause of bilateral blindness and results from the loss of transparency of the lens. Maintenance of the unique tissue architecture of the lens is vital for keeping the lens transparent. Membrane transport mechanisms utilizing several magnesium (Mg)-dependent ATPases, play an important role in maintaining lens homeostasis. Therefore, in Mg-deficiency states, ATPase dysfunctions lead to intracellular depletion of K + and accumulation of Na + and Ca 2+. High intracellular Ca 2+ causes activation of the enzyme calpain II, which leads to the denaturation of crystallin, the soluble lens protein required for maintaining the transparency of the lens. Mg deficiency also interferes with ATPase functions by causing cellular ATP depletion. Furthermore, Mg deficiency enhances lenticular oxidative stress by increased production of free radicals and depletion of antioxidant defenses. Therefore, Mg supplementation may be of therapeutic value in preventing the onset and progression of cataracts in conditions associated with Mg deficiency.