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166. Mitochondrial Nitric Oxide Synthesis During Plant-Pathogen Interactions: Role of Nitrate Reductase in Providing Substrates.

Author

Lamattina, Lorenzo, Polacco, Joseph C., Salgado, Ione, Modolo, Luzia V., Augusto, Ohara, Braga, Márcia R., and Oliveira, Halley C.

Abstract

Nitric oxide (.NO) is an important signaling molecule that regulates plant metabolism and mediates defense responses against biotic and abiotic stresses. Although the cellular mechanisms by which .NO is generated in plants have been intensively investigated, they still remain controversial, particularly those implicated in plant resistance to pathogens. .NO can be synthesized in plants via the oxidation of l-arginine into l-citrulline by a nitric oxide synthase (NOS) that has no homology with the animal NOS family. In addition to l-arginine, nitrite is also an important source for .NO in plants. Since nitrate reductase (NR) activity is required for .NO production, reduction of nitrite catalyzed by the enzyme has been considered a major .NO source in plants. Recent experimental data, however, indicate that NR-defective mutant plants can synthesize .NO from exogenous nitrite. Nevertheless, NR-deficient plants lack enough endogenous substrates (l-arginine and nitrite) for adequate .NO synthesis, resulting in an impaired hypersensitive response (HR). These findings indicate that NR activity is an important source of substrates for .NO production. The main pathways for .NO production from l-arginine and nitrite in plants are located in mitochondria, suggesting that these organelles play a central role in .NO signaling. [ABSTRACT FROM AUTHOR]

Published
2007
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195. Tempol Moderately Extends Survival in a hSOD1G93A ALS Rat Model by Inhibiting Neuronal Cell Loss, Oxidative Damage and Levels of Non-Native hSOD1G93A Forms.

Author

Linares, Edlaine, Seixas, Luciana V., dos Prazeres, Janaina N., Ladd, Fernando V. L., Ladd, Aliny A. B. L., Coppi, Antonio A., and Augusto, Ohara

Subjects
AMYOTROPHIC lateral sclerosis, LABORATORY rats, CELL death, OXIDATIVE stress, MOTOR neurons, ANTIOXIDANTS, CLINICAL trials, PHARMACEUTICAL chemistry
Abstract

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the progressive dysfunction and death of motor neurons by mechanisms that remain unclear. Evidence indicates that oxidative mechanisms contribute to ALS pathology, but classical antioxidants have not performed well in clinical trials. Cyclic nitroxides are an alternative worth exploring because they are multifunctional antioxidants that display low toxicity in vivo. Here, we examine the effects of the cyclic nitroxide tempol (4-hydroxy-2,2,6,6-tetramethyl piperidine-1-oxyl) on ALS onset and progression in transgenic female rats over-expressing the mutant hSOD1G93A . Starting at 7 weeks of age, a high dose of tempol (155 mg/day/rat) in the rat´s drinking water had marginal effects on the disease onset but decelerated disease progression and extended survival by 9 days. In addition, tempol protected spinal cord tissues as monitored by the number of neuronal cells, and the reducing capability and levels of carbonylated proteins and non-native hSOD1 forms in spinal cord homogenates. Intraperitoneal tempol (26 mg/rat, 3 times/week) extended survival by 17 days. This group of rats, however, diverted to a decelerated disease progression. Therefore, it was inconclusive whether the higher protective effect of the lower i.p. dose was due to higher tempol bioavailability, decelerated disease development or both. Collectively, the results show that tempol moderately extends the survival of ALS rats while protecting their cellular and molecular structures against damage. Thus, the results provide proof that cyclic nitroxides are alternatives worth to be further tested in animal models of ALS. [ABSTRACT FROM AUTHOR]

Published
2013
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198. Saccharomyces cerevisiae coq10 null mutants are responsive to antimycin A.

Author

Busso, Cleverson, Tahara, Erich B., Ogusucu, Renata, Augusto, Ohara, Ferreira-Junior, Jose Ribamar, Tzagoloff, Alexander, Kowaltowski, Alicia J., and Barros, Mario H.

Subjects
SACCHAROMYCES cerevisiae, GENETIC mutation, CYTOCHROME c, CHEMICAL reduction, UBIQUINONES
Abstract

Deletion of COQ10 in Saccharomyces cerevisiae elicits a respiratory defect characterized by the absence of cytochrome c reduction, which is correctable by the addition of exogenous diffusible coenzyme Q2. Unlike other coq mutants with hampered coenzyme Q6 (Q6) synthesis, coq10 mutants have near wild-type concentrations of Q6. In the present study, we used Q-cycle inhibitors of the coenzyme QH2-cytochrome c reductase complex to assess the electron transfer properties of coq10 cells. Our results show that coq10 mutants respond to antimycin A, indicating an active Q-cycle in these mutants, even though they are unable to transport electrons through cytochrome c and are not responsive to myxothiazol. EPR spectroscopic analysis also suggests that wild-type and coq10 mitochondria accumulate similar amounts of Q6 semiquinone, despite a lower steady-state level of coenzyme QH2-cytochrome c reductase complex in the coq10 cells. Confirming the reduced respiratory chain state in coq10 cells, we found that the expression of the Aspergillus fumigatus alternative oxidase in these cells leads to a decrease in antimycin-dependent H2O2 release and improves their respiratory growth. [ABSTRACT FROM AUTHOR]

Published
2010
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199. Tempol ameliorates murine viral encephalomyelitis by preserving the blood–brain barrier, reducing viral load, and lessening inflammation

Author

Tsuhako, Maria Heloisa, Augusto, Ohara, Linares, Edlaine, Chadi, Gerson, Giorgio, Selma, and Pereira, Carlos A.

Subjects
*ANTIOXIDANTS, *ENCEPHALOMYELITIS, *LABORATORY mice, *BLOOD-brain barrier, *VIRAL load, *INFLAMMATION, *MULTIPLE sclerosis, *DEMYELINATION
Abstract

Abstract: Multiple sclerosis (MS) is a progressive inflammatory and/or demyelinating disease of the human central nervous system (CNS). Most of the knowledge about the pathogenesis of MS has been derived from murine models, such as experimental autoimmune encephalomyelitis and viral encephalomyelitis. Here, we infected female C57BL/6 mice with a neurotropic strain of the mouse hepatitis virus (MHV-59A) to evaluate whether treatment with the multifunctional antioxidant tempol (4-hydroxy-2,2,6,6-tetramethyl-1-piperidinyloxy) affects the ensuing encephalomyelitis. In untreated animals, neurological symptoms developed quickly: 90% of infected mice died 10 days after virus inoculation and the few survivors presented neurological deficits. Treatment with tempol (24 mg/kg, ip, two doses on the first day and daily doses for 7 days plus 2 mM tempol in the drinking water ad libitum) profoundly altered the disease outcome: neurological symptoms were attenuated, mouse survival increased up to 70%, and half of the survivors behaved as normal mice. Not surprisingly, tempol substantially preserved the integrity of the CNS, including the blood–brain barrier. Furthermore, treatment with tempol decreased CNS viral titers, macrophage and T lymphocyte infiltration, and levels of markers of inflammation, such as expression of inducible nitric oxide synthase, transcription of tumor necrosis factor-α and interferon-γ, and protein nitration. The results indicate that tempol ameliorates murine viral encephalomyelitis by altering the redox status of the infectious environment that contributes to an attenuated CNS inflammatory response. Overall, our study supports the development of therapeutic strategies based on nitroxides to manage neuroinflammatory diseases, including MS. [Copyright &y& Elsevier]

Published
2010
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