Melatonin Protects Tobacco Suspension Cells against Pb-Induced Mitochondrial Dysfunction

Recent studies have shown that melatonin is an important molecule in plant physiology. It seems that the most important is that melatonin effectively eliminates oxidative stress (direct and indirect antioxidant) and switches on different defence strategies (preventive and interventive actions) during environmental stresses. In the presented report, exogenous melatonin potential to protect Nicotiana tabacum L. line Bright Yellow 2 (BY-2) exposed to lead against death was examined. Analyses of cell proliferation and viability, the level of intracellular calcium, changes in mitochondrial membrane potential (ΔΨm) as well as possible translocation of cytochrome c from mitochondria to cytosol and subsequent caspase-like proteolytic activity were conducted. Our results indicate that pretreatment BY-2 with melatonin protected tobacco cells against mitochondrial dysfunction and caspase-like activation caused by lead. The findings suggest the possible role of this indoleamine in the molecular mechanism of mitochondria, safeguarding against potential collapse and cytochrome c release. Thus, it seems that applied melatonin acted as an effective factor, promoting survival and increasing plant tolerance to lead.

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Possible Role of Peroxynitrite in the Responses Induced by Fusicoccin in Plant Cultured Cells

Plants ◽

10.3390/plants10010182 ◽

2021 ◽

Vol 10 (1) ◽

pp. 182 ◽

Cited By ~ 1

Author(s):

Massimo Malerba ◽

Raffaella Cerana

Keyword(s):

Cytochrome C ◽

Dna Fragmentation ◽

Stress Responses ◽

Molecular Chaperones ◽

Caspase 3 ◽

Cultured Cells ◽

Acer Pseudoplatanus ◽

Cytochrome C Release ◽

Induced Stress

Fusicoccin (FC) is a well-known phytotoxin able to induce in Acer pseudoplatanus L. (sycamore) cultured cells, a set of responses similar to those induced by stress conditions. In this work, the possible involvement of peroxynitrite (ONOO−) in FC-induced stress responses was studied measuring both in the presence and in the absence of 2,6,8-trihydroxypurine (urate), a specific ONOO− scavenger: (1) cell death; (2) specific DNA fragmentation; (3) lipid peroxidation; (4) production of RNS and ROS; (5) activity of caspase-3-like proteases; and (6) release of cytochrome c from mitochondria, variations in the levels of molecular chaperones Hsp90 in the mitochondria and Hsp70 BiP in the endoplasmic reticulum (ER), and of regulatory 14-3-3 proteins in the cytosol. The obtained results indicate a role for ONOO− in the FC-induced responses. In particular, ONOO− seems involved in a PCD form showing apoptotic features such as specific DNA fragmentation, caspase-3-like protease activity, and cytochrome c release from mitochondria.

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Calphostin C-mediated translocation and integration of Bax into mitochondria induces cytochrome c release before mitochondrial dysfunction

Cell Death and Differentiation ◽

10.1038/sj.cdd.4400682 ◽

2000 ◽

Vol 7 (6) ◽

pp. 511-520 ◽

Cited By ~ 25

Author(s):

H Ikemoto ◽

E Tani ◽

I Ozaki ◽

H Kitagawa ◽

N Arita

Keyword(s):

Cytochrome C ◽

Mitochondrial Dysfunction ◽

Cytochrome C Release ◽

Calphostin C

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Role of hypoxia-induced Bax translocation and cytochrome c release in reoxygenation injury

Oncogene ◽

10.1038/sj.onc.1202590 ◽

1998 ◽

Vol 17 (26) ◽

pp. 3401-3415 ◽

Cited By ~ 226

Author(s):

Pothana Saikumar ◽

Zheng Dong ◽

Yogi Patel ◽

Kristi Hall ◽

Ulrich Hopfer ◽

...

Keyword(s):

Cytochrome C ◽

Cytochrome C Release ◽

Reoxygenation Injury

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The role of cytochrome c in caspase activation in Drosophila melanogaster cells

The Journal of Cell Biology ◽

10.1083/jcb.200111107 ◽

2002 ◽

Vol 156 (6) ◽

pp. 1089-1098 ◽

Cited By ~ 133

Author(s):

Loretta Dorstyn ◽

Stuart Read ◽

Dimitrios Cakouros ◽

Jun R. Huh ◽

Bruce A. Hay ◽

...

Keyword(s):

Cytochrome C ◽

Mammalian Cells ◽

Significant Proportion ◽

Ectopic Expression ◽

Caspase Activation ◽

Cytochrome C Release ◽

Cell Extracts ◽

Effector Caspase ◽

Drosophila Cells

The release of cytochrome c from mitochondria is necessary for the formation of the Apaf-1 apoptosome and subsequent activation of caspase-9 in mammalian cells. However, the role of cytochrome c in caspase activation in Drosophila cells is not well understood. We demonstrate here that cytochrome c remains associated with mitochondria during apoptosis of Drosophila cells and that the initiator caspase DRONC and effector caspase DRICE are activated after various death stimuli without any significant release of cytochrome c in the cytosol. Ectopic expression of the proapoptotic Bcl-2 protein, DEBCL, also fails to show any cytochrome c release from mitochondria. A significant proportion of cellular DRONC and DRICE appears to localize near mitochondria, suggesting that an apoptosome may form in the vicinity of mitochondria in the absence of cytochrome c release. In vitro, DRONC was recruited to a >700-kD complex, similar to the mammalian apoptosome in cell extracts supplemented with cytochrome c and dATP. These results suggest that caspase activation in insects follows a more primitive mechanism that may be the precursor to the caspase activation pathways in mammals.

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Chenodeoxycholate induction of mitochondrial permeability transition pore is associated with increased membrane fluidity and cytochrome c release: protective role of carvedilol

Mitochondrion ◽

10.1016/s1567-7249(03)00007-2 ◽

2003 ◽

Vol 2 (4) ◽

pp. 305-311 ◽

Cited By ~ 19

Author(s):

Anabela P. Rolo ◽

Paulo J. Oliveira ◽

Antonio J. Moreno ◽

Carlos M. Palmeira

Keyword(s):

Cytochrome C ◽

Membrane Fluidity ◽

Mitochondrial Permeability Transition Pore ◽

Mitochondrial Permeability Transition ◽

Permeability Transition Pore ◽

Permeability Transition ◽

Protective Role ◽

Cytochrome C Release ◽

Mitochondrial Permeability

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Ischemic Preconditioning Is Capable of Inducing Mitochondrial Tolerance in the Rat Brain

Anesthesiology ◽

10.1097/00000542-200210000-00022 ◽

2002 ◽

Vol 97 (4) ◽

pp. 896-901 ◽

Cited By ~ 23

Author(s):

Ren-Zhi Zhan ◽

Hideyoshi Fujihara ◽

Hiroshi Baba ◽

Tomohiro Yamakura ◽

Koki Shimoji

Keyword(s):

Cerebral Ischemia ◽

Cytochrome C ◽

Mitochondrial Dysfunction ◽

Ischemic Preconditioning ◽

Neuronal Death ◽

Brain Mitochondria ◽

Sham Operation ◽

Cytochrome C Release ◽

Hippocampal Ca1 ◽

Ischemic Episode

Background Preconditioning to ischemia is a phenomenon whereby a brief episode of sublethal ischemia and other nonlethal stressors produce protection against a subsequent detrimental ischemic insult. As mitochondrial dysfunction is related to necrotic and apoptotic neuronal death after cerebral ischemia, the authors examined if ischemic preconditioning is capable of inducing mitochondrial tolerance. Methods Forebrain ischemia was induced by bilateral common carotid artery occlusion with simultaneous hypotension for 8 min in Wistar rats (275-300 g). A 3-min ischemic episode performed 48 h before the 8-min ischemia was used for preconditioning. The extents of hippocampal CA1 neuronal damage were evaluated 7 days after reperfusion by neuro-specific nuclear protein immunostaining. Brain mitochondria were isolated 48 h after animals were subjected to the sham operation or the 3-min conditioning ischemia. Loss of cytochrome c from mitochondria after cerebral ischemia in vivo and after exposure of brain mitochondria to calcium in vitro was used as an indication of mitochondrial dysfunction. Results Results showed that ischemic preconditioning induced by a 3-min ischemic episode dramatically reduced the loss of hippocampal CA1 neurons resulting from a subsequent 8-min ischemia 7 days after reperfusion, and this protection was associated with a preservation of mitochondrial cytochrome c as examined after early reperfusion. Exposure of isolated brain mitochondria to calcium produced a dose-dependent increase in cytochrome c release either at 30 degrees C or at 37 degrees C. Compared with those animals receiving only sham operation, cytochrome c release caused by 100 microm calcium was significantly reduced in conditioned animals. Conclusion Regarding the importance of mitochondrial dysfunction in mediating ischemic neuronal death, the above results indicate that mitochondria may serve as end-effecting organelles to ischemic preconditioning.

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