RESUMO
PURPOSE: The purpose of this study was to investigate the oxidative stress response to a short duration bout of submaximal exercise in a cohort of healthy young adults. METHODS: 15 apparently healthy college age males and females completed a modified Bruce-protocol treadmill test to 75-80% of their heart rate reserve. Blood samples collected immediately before (pre-exercise), immediately after, 30, 60 and 120 minutes post-exercise were assayed for total antioxidant capacity (TAC), superoxide disumutase (SOD), thiobarbituric acid-reactive substances (TBARS), and protein carbonyls (PC). RESULTS: SOD activity was significantly increased from pre-exercise levels at 30 minutes (77%), 60 minutes (33%), and 120 minutes (37%) post-exercise. TAC levels were also significantly increased from pre-exercise levels at 60 minutes (30%) and 120 minutes (33%) post-exercise. There were no significant changes in biomarkers for reactive oxygen/nitrogen species (RONS) mediated damage (TBARS and PC) across all post-exercise time points. CONCLUSIONS: In a cohort of healthy young adults, a short duration bout of submaximal aerobic exercise elicited increases in antioxidant activity/concentration, but did not evoke changes in oxidative stress-induced damage. These results may suggest that: (1) short duration bouts of submaximal aerobic exercise are sufficient to induce RONS generation; and (2) the antioxidant defense system is capable of protecting against enhanced RONS production induced by a short duration, submaximal exercise bout in healthy young adults.
RESUMO
Genetic predisposition, particularly specific mitochondrial DNA (mtDNA) backgrounds, has been proposed as a contributing factor in the expression of an epidemic of bilateral optic neuropathy that has affected residents of Cuba since 1991. To substantiate or refute the possibility that specific subsets of mtDNAs could participate in disease expression, we took advantage of the heterogeneous ethnic origin of the Cuban population and the recent identification of a number of mtDNA polymorphisms that appear to be specific for Africans, Native Americans, and Europeans. The screening of both carefully selected people with epidemic neuropathy and control subjects from the Pinar del Rio Province for these polymorphisms revealed that African, Native American, and European mtDNA haplotypes were equally represented among case and control subjects, and suggested that approximately 50% of Cuban mtDNAs originated from Europeans, 46% from Africans, and 4% from Native Americans. These findings demonstrate that mutations arising in specific mtDNAs are unlikely to play a role in the epidemic neuropathy and indicate that analysis of mtDNA haplotypes can be a valuable tool for assessing the relative maternal contribution of Africans, Native Americans, and Europeans in a mixed population.
Assuntos
DNA Mitocondrial/análise , Surtos de Doenças , Doenças do Nervo Óptico/epidemiologia , Doenças do Nervo Óptico/genética , África/etnologia , Cuba/epidemiologia , Europa (Continente)/etnologia , Marcadores Genéticos , Haplótipos , Humanos , Indígenas Norte-Americanos/genética , Reação em Cadeia da Polimerase , Polimorfismo GenéticoRESUMO
An epidemic neuropathy in Cuba has caused bilateral optic neuropathies in more than 26,000 people during the past three years. Various pathogenetic factors have been proposed, including toxins, nutritional deficiencies, and an underlying genetic predisposition involving mitochondrial DNA. As part of a case-control collaborative investigation, 135 Cuban blood samples were analyzed for the most common mitochondrial DNA mutations associated with Leber's hereditary optic neuropathy. None of the participants tested were found to have the mitochondrial DNA mutations at nucleotide positions 11778, 3460, 14484, 7444, or 9804. Of 57 definite case subjects and 69 normal control subjects, three case and three control subjects had the mutation at nucleotide position 9438, three different case and three different control subjects had the mutation at position 13708, and one case and one control subject had the mutation at position 15257 in association with the mutation at position 13708. The most common mitochondrial DNA mutations associated with Leber's hereditary optic neuropathy do not appear to be contributing factors in the epidemic neuropathy in Cuba. We also identified a large Cuban family with maternally related members who experienced visual loss consistent with the diagnosis of Leber's hereditary optic neuropathy. Maternal family members harbored the highly pathogenetic mutation at nucleotide position 11778.
Assuntos
Surtos de Doenças , Atrofias Ópticas Hereditárias/genética , Doenças do Nervo Óptico/epidemiologia , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Criança , Cuba/epidemiologia , DNA Mitocondrial , Eletroforese em Gel de Ágar , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Mutação , Atrofias Ópticas Hereditárias/epidemiologia , Atrofias Ópticas Hereditárias/etiologia , Doenças do Nervo Óptico/etiologia , Doenças do Nervo Óptico/genética , Linhagem , Reação em Cadeia da PolimeraseRESUMO
In laboratory tests, four different strains of Mesocyclops aspericornis (Daday) collected in or near Fortaleza, Brazil, showed potential as biological control agents of Aedes aegypti (L.) mosquito larvae but were not as effective against Anopheles or Culex. In contrast, the larger M. longisetus (Thiebaud), collected at Fortaleza, killed 100% of Ae. aegypti and Anopheles farauti (Laveran) (No. 1) at larval densities of 200/liter and Culex quinquefasciatus (Say) at 25/liter. In cage simulations with Ae. aegypti and Mesocyclops, both copepod species eliminated all immatures in earthenware pots by week 3. Owing to the lack of replacement, all Ae. aegypti adults subsequently died by week 8 or 9. Although both M. longisetus and M. aspericornis showed maximum reproductive potential at 25 degrees C, breeding occurred from 20 to 35 degrees C. Based on these laboratory evaluations, M. longisetus has been selected for field trials in rural villages in Ceará to control Ae. aegypti.