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Virus-induced permeability transition in mitochondria
L D Zorova1, B F Krasnikov, A E Kuzminova
1A.N. Belozersky Institute of Physico-Chemical Biology, Moscow State University, Russia.
Abstract:
Isolated rat liver mitochondria undergo permeability transition after supplementation with a suspension of tobacco mosaic virus. Four mitochondrial parameters proved the opening of the permeability transition pore in the inner mitochondrial membrane: increased oxygen consumption, collapse of the membrane potential, release of calcium ions from mitochondria, and high amplitude mitochondrial swelling. All virus-induced changes in mitochondria were prevented by cyclosporin A. These effects were not observed if the virus was treated with EGTA or disrupted by heating. Protein component of the virus particle in the form of 20S aggregate A-protein, or helical polymer, as well as supernatant of the heat-disrupted virus sample, had no effect on mitochondrial functioning. Electron microscopy revealed the direct interaction of the virus particles with isolated mitochondria. The possible role of the mitochondrial permeability transition pore in virus-induced apoptosis is discussed.
Insights
Tobacco mosaic virus triggers mitochondrial permeability transition in isolated rat liver mitochondria. This virus-induced effect, involving pore opening, was blocked by cyclosporin A, suggesting a role in apoptosis.
Area of Science:
- Biochemistry
- Cell Biology
- Virology
Background:
- Mitochondria play a crucial role in cellular energy production and apoptosis.
- The mitochondrial permeability transition pore (MPTP) is a key regulator of mitochondrial function and cell death.
- Viruses can interact with host cell components, potentially influencing mitochondrial integrity.
Purpose of the Study:
- To investigate the effect of tobacco mosaic virus (TMV) on isolated rat liver mitochondria.
- To determine if TMV can induce mitochondrial permeability transition.
- To explore the potential role of MPTP in virus-induced mitochondrial dysfunction.
Main Methods:
- Isolated rat liver mitochondria were incubated with TMV suspension.
- Mitochondrial parameters including oxygen consumption, membrane potential, calcium ion release, and swelling were measured.
- Electron microscopy was used to visualize virus-mitochondria interactions.
- Cyclosporin A was used to assess the involvement of MPTP.
Main Results:
- TMV supplementation induced mitochondrial permeability transition, evidenced by increased oxygen consumption, membrane potential collapse, calcium release, and swelling.
- Cyclosporin A effectively prevented all TMV-induced mitochondrial changes.
- EGTA treatment or heat disruption of TMV abolished its effects on mitochondria.
- Specific viral protein components or disrupted virus supernatant did not affect mitochondrial function.
Conclusions:
- Tobacco mosaic virus directly interacts with and disrupts mitochondrial function by opening the MPTP.
- The observed mitochondrial dysfunction is dependent on the structural integrity of the virus.
- These findings suggest a potential mechanism for virus-induced apoptosis mediated by MPTP opening.