cytochrome-c-t and maduramicin

cytochrome-c-t has been researched along with maduramicin* in 1 studies

Other Studies

1 other study(ies) available for cytochrome-c-t and maduramicin

Article	Year
Maduramicin induces apoptosis in chicken myocardial cells via intrinsic and extrinsic pathways. Toxicology in vitro : an international journal published in association with BIBRA, 2018, Volume: 50 Maduramicin is one of the most extensively used anticoccidial drugs for the treatment of Eimeria spp. infections. However, overdosage, misuse and drug interactions have resulted in the development of ionophore toxic syndrome. Heart and skeletal muscles have been identified as the main target organs of toxicity. In the present study, primary chicken myocardial cells were isolated to investigate the toxicity and underlying mechanisms of maduramicin. Our results showed that maduramicin causes morphological changes and a decrease in the viability of chicken myocardial cells. Annexin V-FITC/PI and 4',6-diamidino-2-phenylindole (DAPI) staining showed a significant increase in the number of apoptotic cells. Furthermore, caspases-3/8/9 were activated at the gene and protein levels and this was accompanied by the upregulation of apoptosis-related genes, including bcl-2, bax, and cytochrome C. Treatment with the pan-caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp (O-Me) fluoromethyl ketone (z-VAD-fmk) ameliorated the apoptosis and cytotoxicity. Furthermore, intracellular Ca Topics: Animals; Anti-Bacterial Agents; Apoptosis; Calcium; Caspases; Cell Survival; Cells, Cultured; Chickens; Cytochromes c; Glutathione; Lactones; Membrane Potential, Mitochondrial; Myocytes, Cardiac; Proto-Oncogene Proteins c-bcl-2; Reactive Oxygen Species	2018

Article

Year

Maduramicin induces apoptosis in chicken myocardial cells via intrinsic and extrinsic pathways.

Toxicology in vitro : an international journal published in association with BIBRA, 2018, Volume: 50

Maduramicin is one of the most extensively used anticoccidial drugs for the treatment of Eimeria spp. infections. However, overdosage, misuse and drug interactions have resulted in the development of ionophore toxic syndrome. Heart and skeletal muscles have been identified as the main target organs of toxicity. In the present study, primary chicken myocardial cells were isolated to investigate the toxicity and underlying mechanisms of maduramicin. Our results showed that maduramicin causes morphological changes and a decrease in the viability of chicken myocardial cells. Annexin V-FITC/PI and 4',6-diamidino-2-phenylindole (DAPI) staining showed a significant increase in the number of apoptotic cells. Furthermore, caspases-3/8/9 were activated at the gene and protein levels and this was accompanied by the upregulation of apoptosis-related genes, including bcl-2, bax, and cytochrome C. Treatment with the pan-caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp (O-Me) fluoromethyl ketone (z-VAD-fmk) ameliorated the apoptosis and cytotoxicity. Furthermore, intracellular Ca

Topics: Animals; Anti-Bacterial Agents; Apoptosis; Calcium; Caspases; Cell Survival; Cells, Cultured; Chickens; Cytochromes c; Glutathione; Lactones; Membrane Potential, Mitochondrial; Myocytes, Cardiac; Proto-Oncogene Proteins c-bcl-2; Reactive Oxygen Species

2018