<abstract xml:lang="en" xmlns="http://www.w3.org/1999/xhtml">Ca2+ accumulation and Ca2+ overloading in mitochondria are responsible for the cell abnormality associated with ischemia and reperfusion injury. The present study was aimed at evaluating the efficacy of the Ca2+ channel blocker amlodipine on the mitochondrial Ca2+ accumulation, mitochondrial antioxidant status and mitochondrial respiratory enzymes in ischemia and reperfusion (I/R) induced liver injury. I/R injury induced mitochondrial damage in rats was assessed in terms of the decrease in activities (<italic>p</italic> &lt; 0.05) of respiratory marker enzymes (malate dehydrogenase, succinate dehydrogenase and NADH dehydrogenase), mitochondrial antioxidant enzymes (glutathione, superoxide dismutase, catalase), and significant increase (<italic>p</italic> &lt; 0.05) in the level of lipid peroxidation (LPO) and Ca2+ content.Mitochondrial damage was confirmed by transmission electron microscopic (TEM) examination. Pretreatment with amlodipine effectively counteracted the alteration in mitochondrial enzymes induced by ischemia-reperfusion liver damage. TEM study confirms the restoration of cellular normalcy and the cytoprotective role of amlodipine against I/R induced hepatic injury. On the basis of our findings it may be concluded that amlodipine not only possesses Ca2+ channel antagonist properties but it may also reduce the extent of mitochondrial damage by its antioxidant activity.</abstract>

Ca2+ accumulation and Ca2+ overloading in mitochondria are responsible for the cell abnormality associated with ischemia and reperfusion injury. The present study was aimed at evaluating the efficacy of the Ca2+ channel blocker amlodipine on the mitochondrial Ca2+ accumulation, mitochondrial antioxidant status and mitochondrial respiratory enzymes in ischemia and reperfusion (I/R) induced liver injury. I/R injury induced mitochondrial damage in rats was assessed in terms of the decrease in activities (p < 0.05) of respiratory marker enzymes (malate dehydrogenase, succinate dehydrogenase and NADH dehydrogenase), mitochondrial antioxidant enzymes (glutathione, superoxide dismutase, catalase), and significant increase (p < 0.05) in the level of lipid peroxidation (LPO) and Ca2+ content.Mitochondrial damage was confirmed by transmission electron microscopic (TEM) examination. Pretreatment with amlodipine effectively counteracted the alteration in mitochondrial enzymes induced by ischemia-reperfusion liver damage. TEM study confirms the restoration of cellular normalcy and the cytoprotective role of amlodipine against I/R induced hepatic injury. On the basis of our findings it may be concluded that amlodipine not only possesses Ca2+ channel antagonist properties but it may also reduce the extent of mitochondrial damage by its antioxidant activity.

Protective role of the calcium channel blocker amlodipine against mitochondrial injury in ischemia and reperfusion injury of rat liver

Cellular and Microbiology Laboratory, College of Pharmacy, IFTM, Moradabad-244001, India

Birla Institute of Technology and Sciences, Pilani, India

National Biotechnology Center, Indian Veterinary Research Institute, Izatnagar India

Acta Pharmaceutica

Ca2+ accumulation and Ca2+ overloading in mitochondria are responsible for the cell abnormality associated with ischemia and reperfusion injury. The present...

Protective role of the calcium channel blocker amlodipine against mitochondrial injury in ischemia and reperfusion injury of rat liver

Publicado en línea: 22 dic 2008

Páginas: 421 - 428

DOI: https://doi.org/10.2478/v10007-008-0022-3

Palabras clave
blokator kalcijevih kanala, amlodipin, ishemična i reperfuzijska ozljeda, oštećenje mitohondrija

This content is open access.

Protective role of the calcium channel blocker amlodipine against mitochondrial injury in ischemia and reperfusion injury of rat liver

Publicado en línea: 22 dic 2008

Páginas: 421 - 428

DOI: https://doi.org/10.2478/v10007-008-0022-3

Palabras claveblokator kalcijevih kanala, amlodipin, ishemična i reperfuzijska ozljeda, oštećenje mitohondrija

This content is open access.

Palabras clave
blokator kalcijevih kanala, amlodipin, ishemična i reperfuzijska ozljeda, oštećenje mitohondrija