Antioxidant capacity and biological activity of essential oil and methanol extract of Conobea scoparioides (Cham. & Schltdl.) Benth

Os óleos essenciais da planta sub-aquática Conobea scoparioides (fresca e previamente seca) apresentaram rendimentos de 3,4 e 3,3%, respectivamente. Os principais constituintes identificados foram o éter metílico do timol (39,6 e 47,7%), timol (40,0 e 26,4%), α-felandreno (12,1 e 14,3%) e p-cimeno (1,5 e 1,7%), totalizando mais de 90% nos referidos óleos. A concentração de seqüestro do radical DPPH (CE50) dos óleos e extrato foi de 46,7 ± 3,6 µg mL^-1 para a planta fresca (CsO-f), de 56,1 ± 2,4 µg mL^-1 para a planta seca (CsO-d), e de 23,0 ± 2,2 µg mL^-1 para o extrato metanólico (CsE-d). O valor do extrato é comparável ao BHT (19,8 ± 0,5 µg mL^-1), usado como padrão antioxidante. O valor médio dos óleos é duas vezes menor, mas igualmente importante como agente antioxidante. O teor de Fenólicos Totais (TP, 124,6 ± 8,7 mg GAE per g) e o Trolox Equivalente (TEAC, 144,1 ± 4,9 mg TE per g) do extrato metanólico confirmaram a significativa atividade antioxidante de C. scoparioides. Da mesma forma, nos bioensaios com larva de camarão (Artemia salina) o valor médio da concentração letal dos óleos (CL₅₀, 7,7 ± 0,3 µg mL^-1) foi dez vezes maior que no extrato metanólico (CL₅₀, 77,6 ± 7,1 µg mL^-1) mostrando importante atividade biológica.

Therapeutic concentration of morphine reduces oxidative stress in glioma cell line

Morphine is a potent analgesic opioid used extensively for pain treatment. During the last decade, global consumption grew more than 4-fold. However, molecular mechanisms elicited by morphine are not totally understood. Thus, a growing literature indicates that there are additional actions to the analgesic effect. Previous studies about morphine and oxidative stress are controversial and used concentrations outside the range of clinical practice. Therefore, in this study, we hypothesized that a therapeutic concentration of morphine (1 μM) would show a protective effect in a traditional model of oxidative stress. We exposed the C6 glioma cell line to hydrogen peroxide (H₂O₂) and/or morphine for 24 h and evaluated cell viability, lipid peroxidation, and levels of sulfhydryl groups (an indicator of the redox state of the cell). Morphine did not prevent the decrease in cell viability provoked by H₂O₂) but partially prevented lipid peroxidation caused by 0.0025% H₂O₂) (a concentration allowing more than 90% cell viability). Interestingly, this opioid did not alter the increased levels of sulfhydryl groups produced by exposure to 0.0025% H₂O₂), opening the possibility that alternative molecular mechanisms (a direct scavenging activity or the inhibition of NAPDH oxidase) may explain the protective effect registered in the lipid peroxidation assay. Our results demonstrate, for the first time, that morphine in usual analgesic doses may contribute to minimizing oxidative stress in cells of glial origin. This study supports the importance of employing concentrations similar to those used in clinical practice for a better approximation between experimental models and the clinical setting.