Role of Intracellular Ca 2+ , Reactive Oxygen Species, Mitochondria Transmembrane Potential, and Antioxidant Enzymes in Heavy Metal-Induced Apoptosis in Fish Cells

Xiang, Li-Xin; Shao, Jian‐Zhong

doi:10.1007/s00128-003-0137-7

Cited by 18 publications

(5 citation statements)

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“…Copper, an integral component of cytochrome oxidase located in the intramitochondrial space and imported by a protein COX17 [29] is tightly bound to this site and is an unlikely candidate. Regarding Cu 2+ , in line with previous observations [4,11], our results indicated that incubation of mitochondria with 10 μm of this cation may have induced a high stimulation of oxygen-derived reactive species [11] that brought about mitochondrial permeability transition pore opening, whereas 5 μM Cu 2+ was unable to induce matrix Ca 2+ efflux from mitochondria and caused permeability transition in a sucrose medium [13]. On the other hand, our results appeared to give support to the widespread knowledge that mitochondria were more susceptible to permeability transition when incubated in potassium medium; Cu 2+ at a low concentration could initiate matrix Ca 2+ release and cause obvious permeability transition.…”

Section: Discussionsupporting

confidence: 92%

High Copper Levels Promotes Broiler Hepatocyte Mitochondrial Permeability Transition In Vivo and In Vitro

Wang

Pan

et al. 2011

Biol Trace Elem Res

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This study was to examine the effects of copper on the mitochondrial non-specific pore. Three hundred sixty, one-day-old, healthy Arbor Acres (AA) broilers were fed with different concentrations (11, 110, 220, and 330 mg/kg) of copper originated from copper sulfate, tribasic copper chloride (TBCC), or copper methionine. At the indicated time point, the mitochondrial permeability transition (MPT) and copper concentration were analyzed. Results showed that under the same copper concentration, the MPT of broilers fed copper methionine was the greatest, followed by TBCC, then copper sulfate. The effects of copper on MPT were time- and dose-dependent. Furthermore, in vitro in the presence of K(+), 5 μM Cu(2+) could cause permeability transition as compared to 10 μM Cu(2+) in buffer without K(+). Taking these results together, we have shown that hepatocellular MPT may be influenced not only by source and concentration of copper or the raising period of broilers, but also by the existence of K(+).

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Section: Discussionsupporting

confidence: 92%

High Copper Levels Promotes Broiler Hepatocyte Mitochondrial Permeability Transition In Vivo and In Vitro

Wang

Pan

et al. 2011

Biol Trace Elem Res

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“…However in regard to the findings described in this manuscript it is possible that the lower ROS production could be due to the onset of apoptosis and thus lower cell numbers in the culture. Reactive oxygen species are known for their cytotoxicity in fish [43,44] and hence it is possible that the higher β-glucan concentrations induced ROS, causing apoptosis which then results in lower respiratory burst activity due to the reduced cell numbers.…”

Section: Discussionmentioning

confidence: 99%

Time and concentration dependency of MacroGard® induced apoptosis

Miest

Hoole

2015

Fish & Shellfish Immunology

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In previous studies an effect of β-glucan on apoptosis in fish was noted and in this investigation we determine the time and concentration dependency of this effect. Primary cell cultures of pronephric carp cells were incubated for 6, 24, 48 h with various concentrations ranging from 0 -1000 μg/ml of MacroGard ® β-glucan. Apoptosis was monitored via acridine orange staining. Results indicate a clear effect of time and concentration on the induction of apoptosis in vitro, with only concentration ≥ 500 μg/ml causing significantly higher percentages of apoptotic cells. Apoptosis was detected after 6 h. This concentration dependent effect has to be considered when studying apoptosis in relation to immunostimulation.

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“…Studies on rat hepatocytes have indicated that the main sources of ROS generation in the presence of copper were the lysosomes [115,116], whereas the mitochondria, a significant source of ROS under basal conditions appeared not to be involved [117,118]. At the same time, however, mitochondria are clearly important targets of metal toxicity and in many cases a close link between metal-induced radical stress and mitochondrial function has been established [119,120]. The induction…”

Section: Apoptosismentioning

confidence: 99%