Effect of Copper Chloride Exposure on the Membrane Potential and Cytosolic Free Calcium in Primary Cultured Chicken Hepatocytes

Abstract

This study was conducted to examine the effects of copper on membrane potential and cytosolic free calcium in isolated primary chicken hepatocytes which were exposed to different concentration of Cu(2+) (0, 10, 50, 100 μM) or a mixture of Cu(2+) and vitamin C (50 and 50 μM, respectively). Viability, membrane potential, and cytosolic free Ca(2+) of monolayer cultured hepatocytes were investigated at the indicated time point. Results showed that, among the different concentrations of Cu(2+) exposure, the viability of hepatocytes treated with 100 μM Cu(2+) was the worst at the 12th and 24th hours. The effects of Cu(2+) on viability and proliferation were time and dose dependent. Further investigation indicated that Cu(2+) exposure significantly enhanced cytosolic free Ca(2+) in hepatocytes, compared to that in control group, at the 24th hour. Meanwhile, membrane potential was noticeably reduced in hepatocytes increasing concentration of Cu(2+). Taking these results together, we have shown that Cu(2+) can cause toxicity to primary chicken hepatocytes in excessive dose and the effect of Cu(2+) exposure on membrane potential is not site specific, which is probably mediated by the changes of cytosolic free Ca(2+).

Antiparasitic effect of copper alloy mesh on tomont stage of Cryptocaryon irritans in aquaculture

“…Additionally, the disturbance in mitochondria has a variety of harmful consequences, including energy shortage, oxidative stress, accumulation of triglycerides and cell death. A previous study also indicated that the toxicity of copper decreases mitochondrial respiration that induces apoptosis, and these findings support recent study that the degradation of mitochondria leads to overwhelming results (Jia et al, 2012).…”

Role of Copper on Mitochondrial Function and Metabolism

“…Copper overload produces liver cirrhosis, neurodegeneration, and anemia mostly via the exacerbation of hydroxyl radical production by the Fenton and Haber-Weiss reactions. Copper toxicity decreases mitochondrial respiration and induces apoptosis (Medeiros and Jennings 2002;Su et al, 2011;Jia et al, 2012). On the other hand, Menkes disease features mutations in the transporter ATP7A which affect the release of copper from the enterocyte to the bloodstream, causing a severe copper deficiency that in most of cases results in death due to CIV and SOD1 dysfunction (Rossi et al, 2004;Horn and Barrientos 2008;Kim et al, 2008;Turski and Thiele 2009).…”