CDP‐choline circumvents mercury‐induced mitochondrial damage and renal dysfunction. (1st October 2017)

• Record Type: Journal Article
• Authors: Buelna‐Chontal, Mabel; Franco, Martha; Hernández‐Esquivel, Luz; Pavón, Natalia; Rodríguez‐Zavala, José S.; Correa, Francisco; Jasso, Ricardo; Pichardo‐Ramos, Gregorio; Santamaría, José; González‐Pacheco, Héctor; Soto, Virgilia; Díaz‐Ruíz, Jorge L.; Chávez, Edmundo
• Is Part Of: Cell biology international. Volume 41:Number 12(2017)
• Page Start: 1356
• Page End: 1366
• Publication Date: 2017-10-01
• Subjects: kidney dysfunction -- mercury -- mitochondria -- permeability transition; Cytology -- Periodicals; Cells -- Periodicals; 571.605
• DOI: 10.1002/cbin.10871
• Languages: English
• ISSNs: 1065-6995

Abstract

Abstract: Heavy metal ions are known to produce harmful alterations on kidney function. Specifically, the accumulation of Hg 2+ in kidney tissue may induce renal failure. In this work, the protective effect of CDP‐choline against the deleterious effects induced by Hg 2+ on renal function was studied. CDP‐choline administered ip at a dose of 125 mg/kg body weight prevented the damage induced by Hg 2+ administration at a dose of 3 mg/kg body weight. The findings indicate that CDP‐choline guards mitochondria against Hg 2+ ‐toxicity by preserving their ability to retain matrix content, such as accumulated Ca 2+ . This nucleotide also protected mitochondria from Hg 2+ ‐induced loss of the transmembrane electric gradient and from the generation of hydrogen peroxide and membrane TBARS. In addition, CDP‐choline avoided the oxidative damage of mtDNA and inhibited the release of the interleukins IL‐1 and IL6, recognized as markers of acute inflammatory reaction. After the administration of Hg 2+ and CDP, CDP‐choline maintained nearly normal levels of renal function and creatinine clearance, as well as blood urea nitrogen (BUN) and serum creatinine.