Navegando por Palavras-chave "Mitochondrial Dysfunction"

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    Pre-exercise led phototherapy (638 nm) prevents grip strength loss in elderly women: a double-blind randomized controlled trial
    (Ios press, 2016) Matos, Areolino Pena; Navarro, Ricardo Scarparo; Lombardi Júnior, Imperio [UNIFESP]; Brugnera, Aldo, Jr.; Munin, Egberto; Villaverde, Antonio Balbin
    BACKGROUND: LED phototherapy can attenuate muscle fatigue and accelerate muscle recovery in young persons, but little is known about photobiomodulation effects on muscle strength in the elderly. OBJECTIVE: To assess the effects of LED phototherapy on the grip strength and muscle fatigue of wrist flexors in elderly women. METHODS: Twenty-nine women were recruited and allocated to Placebo Group (PG) (n = 14) and LED Group (LG) (n = 15). Grip strength, number of resisted wrist flexion repetitions, and serum creatine kinase (CK) were measured. The subjects were irradiated with one diode (638 nm, 150 mW, 11.7 J/cm(2), 4.5 J/point) at four points on the wrist flexor muscles, and fatigue was induced by exercise using 75% of one maximum repetition (1MR). When muscle fatigue was reached, grip strength and CK were reassessed. RESULTS: In the LG, there was no intra-group difference for grip strength (N), 217.7 +/- 34.3 to 209.9 +/- 35.3 (p = 0.063) whereas in the PG, there was decrease in strength from 203.0 +/- 22.5 to 181.4 +/- 21.6 (p < 0.001). LED increased the number of repetitions by 22.0%. An increase in CK (U/L) was observed in PG in all post-fatigue periods (p = 0.003) but no difference was found in the LG (p = 0.972). CONCLUSIONS: A single application of LED before muscle fatigue induction may effectively maintain grip strength and reduce muscle fatigue and damage.
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    The Role of Mitochondrial Function in Glutamate-Dependent Metabolism in Neuronal Cells
    (Bentham Science Publ Ltd, 2011-12-01) Smaili, Soraya Soubhi [UNIFESP]; Ureshino, Rodrigo Portes [UNIFESP]; Rodrigues, L. [UNIFESP]; Rocha, Katiucha Karolina [UNIFESP]; Carvalho, J. T. [UNIFESP]; Oseki, Karen Tubono [UNIFESP]; Bincoletto, Claudia [UNIFESP]; Lopes, Guiomar Silva [UNIFESP]; Hirata, Hanako [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Glutamate is an important neurotransmitter in neurons and glial cells and it is one of the keys to the neuron-glial interaction in the brain. Glutamate transmission is strongly dependent on calcium homeostasis and on mitochondrial function. In the present work we presented several aspects related to the role of mitochondria in glutamate signaling and in brain diseases. We focused on glutamate-induced calcium signaling and its relation to the organelle dysfunction with cell death processes. In addition, we have discussed how alterations in this pathway may lead or aggravate a variety of neurodegenerative diseases. We compiled information on how mitochondria can influence cell fate during glutamate stimulation and calcium signaling. These organelles play a pivotal role in neuron and glial exchange, in synaptic plasticity and several pathological conditions related to Aging, Alzheimer's, Parkinson's and Huntington's diseases. We have also presented autophagy as a mechanism activated during mitochondrial dysfunction which may function as a protective mechanism during injury. Furthermore, some new perspectives and approaches to treat these neurodegenerative diseases are offered and evaluated.