Desipramine Ameliorates Cr(VI)-Induced Hepatocellular Apoptosis via the Inhibition of Ceramide Channel Formation and Mitochondrial PTP Opening | Zendy

Luo Lei | Zendy; Ying Xie | Zendy; An Wang | Zendy; Xinmin Liu | Zendy; Fang Xiao | Zendy; Xiali Zhong | Zendy; Caigao Zhong | Zendy

Open Access

Desipramine Ameliorates Cr(VI)-Induced Hepatocellular Apoptosis via the Inhibition of Ceramide Channel Formation and Mitochondrial PTP Opening

Author(s) -

Luo Lei,

Ying Xie,

An Wang,

Xinmin Liu,

Fang Xiao,

Xiali Zhong,

Caigao Zhong

Publication year - 2014

Publication title -

cellular physiology and biochemistry

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.486

H-Index - 87

eISSN - 1421-9778

pISSN - 1015-8987

DOI - 10.1159/000369657

Subject(s) - ceramide , acid sphingomyelinase , apoptosis , sphingomyelin phosphodiesterase , sphingomyelin , chemistry , mitochondrial permeability transition pore , desipramine , mitochondrion , microbiology and biotechnology , biochemistry , programmed cell death , biology , endocrinology , cholesterol , hippocampus , antidepressant

Hexavalent chromium (Cr(VI)) is a common environmental pollutant. Cr(VI) exposure can lead to severe damage in the liver, but the preventive measures to diminish Cr(VI)-induced hepatotoxicity need further study. Acid sphingomyelinase (ASMase) is responsible for the production of ceramide via the hydrolysis of sphingomyelin. The present study was designed to investigate effects of desipramine (DES), as an ASMase inhibitor, on Cr(VI)-induced hepatotoxicity.

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