Action of cyclosporine on mitochondrial calcium fluxes

Fournier, Nancy; Ducet, Gaston; Crevat, A.

doi:10.1007/bf00762419

Cited by 317 publications

(156 citation statements)

References 10 publications

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“…This finding is in agreement with the findings of the studies done by Turk et al (2007Turk et al ( , 2010. The increment in MDA levels are probably because of the extreme generation of ROS by blocking the permeability transition pore, providing an increase in Ca 2+ concentration, and distruption of mitochondrial electron transport chain (Fournier et al, 1987;Nicolli et al, 1996). When ROS began to be kept under control, testes exhibit a defensive mechanism using different antioxidant enzymes.…”

Section: Discussionsupporting

confidence: 91%

The effects of propolis on sperm quality, reproductive organs and testicular antioxidant status of male rats treated with cyclosporine-A

Baykalır¹,

Seven²,

Gür³

et al. 2016

Anim Reprod

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This study was designed to determine the effects of propolis on the quality of sperm and reproductive organs in male rats treated with cyclosporine-A. In this study, 24 male Sprague-Dawley rats (280-300 g BW) at 8-10 weeks of age were used. The rats were randomly divided into control and 3 treatment groups. Each rat was placed into a cage. During 21 days (experimental period), Group 1 served as control group; Group 2 (CsA) was given 15 mg/kg BW/day of CsA by subcutaneously; Group 3 (P) was given 100 mg/kg BW/day of propolis by gavage; Group 4 (CsA+P) was given 15 mg/kg BW/day of CsA subcutaneously and 100 mg/kg BW/day of propolis by gavage. Administration of CsA to rats decreased sperm motility (P < 0.01) and sperm concentration (P < 0.01), and it increased total abnormal sperm rates (P < 0.05) as compared with the control group. Significant improvements were observed in the sperm motility (P < 0.01) and total abnormal sperm rates (P < 0.05) in CsA+P group. No significant differences were observed in the weights of right and left testes among all groups. The weight values of right and left epididymis were found similar to each other in CsA administrated groups. Seminal vesicle (P < 0.01) and prostat glands weights (P < 0.01) were significantly higher in CsA+P group than CsA group. As a result, it was determined that oral supplementation of 100 mg/kg of propolis had amendatory effect on the quality of sperm and reproductive organs treated with CsA administered rats. CsA treatment caused a significant increase in MDA level (P < 0.01) and significant decreases (P < 0.01) in GSH level and CAT activity when compared with the control group. Ingestion of propolis by CsA-treated rats significantly decreased the MDA level and significantly increased the GSH level when compared with the CsA alone group (P < 0.01).

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Section: Discussionsupporting

confidence: 91%

The effects of propolis on sperm quality, reproductive organs and testicular antioxidant status of male rats treated with cyclosporine-A

Baykalır¹,

Seven²,

Gür³

et al. 2016

Anim Reprod

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“…Fig. 6B shows the ability of 5 M CyA and 50 M ArA to prevent cell death from taking place in the presence of different concentrations of rotenone during 15 and 30 h. CyA inhibits the opening of the MPT pore (32), and phospholipase A2 inhibitors, such as ArA, enhance and prolong this effect (30,31). Because CyA is not able to maintain mitochondrial function, it did not prevent rotenone-induced apoptosis after long periods of rotenone treatment.…”

Section: Effect Of CI Inhibition On Cell Deathmentioning

confidence: 99%

Titrating the Effects of Mitochondrial Complex I Impairment in the Cell Physiology

Barrientos

Moraes

1999

Journal of Biological Chemistry

356

217

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The mitochondrial oxidative phosphorylation system consists of five multimeric enzymes (complexes I-V). NADH dehydrogenase or complex I (CI) is affected in most of the mitochondrial diseases and in some neurodegenerative disorders. We have studied the physiological consequences of a partial CI inhibition at the cellular level. We used a genetic model (40% CI-inhibited human-ape xenomitochondrial cybrids) and a drug-induced model (0 -100% CI-inhibited cells using different concentrations of rotenone). We observed a quantitative correlation between the level of CI impairment and cell respiration, cell growth, free radical production, lipid peroxidation, mitochondrial membrane potential, and apoptosis. We showed that cell death was quantitatively associated with free radical production rather than with a decrease in respiratory chain function. The results obtained with human xenomitochondrial cybrid cells were compatible with those observed in rotenoneinduced 40% CI-inhibited cells. At high concentrations (5-6-fold higher than the concentration necessary for 100% CI inhibition), rotenone showed a second toxic effect at the level of microtubule assembly, which also led to apoptosis. The correlation found among all the parameters studied helped clarify the physiological consequences of partial CI inhibitions at the cellular level.

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“…23 and 24). The immunosuppressive cyclic endecapeptide, cyclosporin A (CsA) specifically blocks the phenomenon (25,26), which is because of the opening of a pore, identified as a non-selective, highly conductive "megachannel" (24). Opening of the transition pore causes a series of events culminating in bioenergetic collapse and a redox catastrophe (11).…”

mentioning

confidence: 99%

Oxidative Stress Is Responsible for Mitochondrial Permeability Transition Induction by Salicylate in Liver Mitochondria

Battaglia

Salvi

Toninello

2005

Journal of Biological Chemistry

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The interaction of salicylate with the respiratory chain of liver mitochondria generates hydrogen peroxide and, most probably, other reactive oxygen species, which in turn oxidize thiol groups and glutathione. This oxidative stress, confirmed by the prevention of action by antioxidant agents, leads to the induction of the mitochondrial permeability transition in the presence of Ca 2؉ . This phenomenon induces further increase of oxidative damage resulting in impairment of oxidative phosphorylation and ␤-oxidation, cardinal features of Reye's syndrome in the liver. Mitochondrial permeability transition induction also induces the release of cytochrome c and apoptotic inducing factor from mitochondria, suggesting that salicylate also behaves as a pro-apoptotic agent. The reactive group of salicylate for inducing oxidative stress is the hydroxyl group which, by interacting with a Fe-S cluster of mitochondrial Complex I, the so-called N-2(Fe-S) center, produces reactive oxygen species.

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Action of cyclosporine on mitochondrial calcium fluxes

Cited by 317 publications

References 10 publications

The effects of propolis on sperm quality, reproductive organs and testicular antioxidant status of male rats treated with cyclosporine-A

The effects of propolis on sperm quality, reproductive organs and testicular antioxidant status of male rats treated with cyclosporine-A

Titrating the Effects of Mitochondrial Complex I Impairment in the Cell Physiology

Oxidative Stress Is Responsible for Mitochondrial Permeability Transition Induction by Salicylate in Liver Mitochondria

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