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Byline: M. A. Asif, M. M. A. Hamid, M. Shoaib, M. A. Mirza, H. H. Iqbal, M. I. Khan, Najam-us-Sahar, S. Ashraf, M. M. Javed, S. Shehzad, M. S. Asif [...]

Nitrophenol isomers (o -nitrophenol, m-nitrophenol, p-nitrophenol) are widely used as analytical reagents or intermediates for a variety of chemicals (for example, in pesticides, medicines, and dyes). Hence, a large amount [...]

Molecular dynamics (MD) simulation of lactic acid (L-acid) and pyruvic acid (P-acid) in a physiological salt solution has been performed, which is used as the electrolyte in a sort of biofuel cell working on a human skin. The structure, frequency distribution of molecules, dielectric properties, rotational correlation functions, and diffusion coefficients have been calculated. The anomalous behavior of dielectric constants for the lower concentration of L-acid and P-acid has been obtained from MD. The anomalous dielectric constant is discussed in relation with the various physical properties of the solution including the life time of the interaction in the solution. MD results suggest that the anomalous behavior is supposed to be attributed to the difference of interactions between ions in the lower and higher concentration region., INTRODUCTION In recent years, natural polymers attract considerable attention, because they are made from waste natural materials. Some natural polymers such as poly lactic acid (L-acid) are suitable for biomedical [...]

Molecular hydrogen ([H.sub.2]) showed protection against various kinds of oxidative-stress-related diseases. First, it was reported that the mechanism of therapeutic effects of [H.sub.2] was antioxidative effect due to inhibition of the most cytotoxic reactive oxygen species, hydroxy radical (*OH). However, after chronic administration of [H.sub.2] in drinking water, oxidative-stress-induced nerve injury is significantly attenuated even in the absence of [H.sub.2]. It suggests indirect signaling of [H.sub.2] and gastrointestinal tract is involved. Indirect effects of [H.sub.2] could be tested by giving [H.sub.2] water only before nerve injury, as preconditioning. For example, preconditioning of [H.sub.2] for certain a period (~7 days) in Parkinson's disease model mice shows significant neuroprotection. As the mechanism of indirect effect, [H.sub.2] in drinking water induces ghrelin production and release from the stomach via [beta]1-adrenergic receptor stimulation. Released ghrelin circulates in the body, being transported across the blood-brain barrier, activates its receptor, growth-hormone secretagogue receptor. [H.sub.2]-induced upregulation of ghrelin mRNA is also shown in ghrelin-producing cell line, SG-1. These observations help with understanding the chronic effects of [H.sub.2] and raise intriguing preventive and therapeutic options using [H.sub.2]. Key words: molecular hydrogen, preconditioning, Parkinson's disease, ghrelin. L'hydrogene moleculaire ([H.sub.2]) est decrit comme etant protecteur contre divers types de maladies liees au stress oxydatif. Il a d'abord ete rapporte que le mode d'action des effets therapeutiques de l'[H.sub.2] etait un effet antioxydant cause par l'inhibition du radical hydroxyl (*OH), le derive reactif de l'oxygene le plus toxique. Cependant, apres l'administration a long terme d'[H.sub.2] dans l'eau a boire, les lesions nerveuses provoquees parle stress oxydatif sont nettement attenuees, meme en absence d'[H.sub.2]. Cela laisse entendre qu'il existerait une voie de signalisation indirecte de l'[H.sub.2] et que le tractus gastro-intestinal jouerait un role. Les effets indirects de l'[H.sub.2] pourraient etre evalues en donnant de l'eau avec [H.sub.2] seulement, avant les lesions nerveuses, en tant que preconditionnement. Par exemple, le preconditionnement par l'[H.sub.2] pendant une certaine periode (~7 jours) dans un modele murin de maladie de Parkinson permet d'obtenir une neuroprotection notable. Comme mode d'action d'un effet indirect, l'[H.sub.2] dans l'eau a boire engendre la production et la liberation de ghreline par l'estomac par l'intermediaire d'une stimulation des recepteurs [beta]1-adrenergiques. La ghreline liberee circule dans l'organisme, transportee a travers la barriere hemo-encephalique, active son recepteur secretagogue d'hormone de croissance (GHSR). Nous observons aussi la regulation a la hausse de l'ARNm de ghreline engendre par l'[H.sub.2] dans des lignees cellulaires productrices de ghreline (SG- 1). Ces observations contribuent a la comprehension des effets a long terme de l'[H.sub.2] et laissent entrevoir d'interessantes options therapeutiques et de prevention fondees sur l'utilisation de l'[H.sub.2]. [Traduit par la Redaction] Mots-cles : hydrogene moleculaire, preconditionnement, maladie de Parkinson, ghreline., Introduction Inhaling molecular hydrogen ([H.sub.2]) showed protection against brain injury induced by focal ischemia and reperfusion in rat by reducing hydroxy radical (*OH), the most toxic reactive oxygen species (Ohsawa [...]

ARTICLE INFO Keywords: Curcumin Intestinal ischemia reperfusion Lung Heart Oxidative stress ABSTRACT The aim of this study was to investigate the effects curcumin on inflammation and oxidative stress markers in [...]

Prolonged stress results in elevation of glucocorticoid (GC) hormones, which can have deleterious effects in the brain. The hippocampus, which has a high concentration of glucocorticoid receptors, is especially vulnerable to increasing levels of GCs. GCs have been suggested to endanger hippocampal neurons by exacerbating the excitotoxic glutamatecalcium--reactive oxygen species (ROS) cascade. In an effort to reveal the mechanisms underlying GC-mediated hippocampal neurotoxicity, we aimed to clarify the molecular pathway of GC-induced ROS increase by using organotypic hippocampal slice cultures. Assays for ROS, using 2',7'-dichlorodihydrofluorescein diacetate fluorescence, showed that treatment of synthetic GC, dexamethasone (DEX) significantly enhanced ROS levels. Time course and dose response analyses indicated that peak amount of ROS was generated at 4 h after treatment with 50 µmol/L DEX. By contrast, other steroid hormones, progesterone and estradiol did not influence ROS production. N-acetyl-L-cysteine completely suppressed ROS produced by DEX. Propidium iodide staining exhibited prominent cell death in the hippocampal layer after 96 h of DEX treatment. RU486, a GC receptor antagonist, almost completely blocked the effect of DEX on ROS production and cell death, indicating that DEX-induced ROS overproduction and hippocampal death are mediated via GC receptors. Real-time reverse transcriptase PCR analysis demonstrated that after DEX treatment the level of glutathione peroxidase mRNA was decreased whereas that of NADPH oxidase mRNA was significantly enhanced. These findings suggest that excess GCs cause hippocampal damage by regulating genes involved in ROS generation. Key words: glucocorticoid, hippocampus, neurotoxicity, organotypic hippocampal slice culture, reactive oxygen species, stress. Un stress prolonge entraine une augmentation d'hormones glucocorticoides (GC), ce qui peut avoir des effets nefastes dans le cerveau. L'hippocampe, qui contient une grande concentration de recepteurs aux glucocorticoides, est particulierement vulnerable a l'augmentation des taux de GC. On a suggere que les GC compromettent la survie des neurones hippocampiques en exacerbant la cascade excitotoxique glutamate-calcium-especes reactives de l'oxygene (ROS). Dans le but d'identifier les mecanismes sous-jacents a la neurotoxicite hippocampique vehiculee par les GC, notre avons utilise des cultures organotypiques de tranches d'hippocampe pour examiner la voie moleculaire de l'augmentation des ROS induite par les CG. Les essais, effectues en utilisant la fluorescence du 1',7'-dichlorodihydrofluoresceine diacetate, ont montre qu'un traitement a la GC synthetique, dexamethasone (DEX), a augmente significativement les taux de ROS. Les analyses de l'evolution temporelle et de la relation dose-reponse ont indique que la production maximale de ROS a eu lieu 4 h apres un traitement avec 50 µ M de DEX. Toutefois, d'autres hormones steroidiennes, progesterone et oestradiol, n'ont pas influe sur la production des ROS. La N-acetyl-L-cysteine a totalement supprime les ROS produites par la DEX. La coloration a l'iodure de propidium a montre une mort cellulaire significative dans la couche hippocampique apres 96 h de traitement a la DEX. RU486, un antagoniste des recepteurs aux GC, a presque completement bloque la production de ROS et la mort des cellules induites par le traitement a la DEX, ce qui indique que la surproduction de ROS et la mort hippocampique induites par la DEX sont vehiculees par les recepteurs aux GC. La technique de RT-PCR en temps reel a demontre que le taux d'ARNm de la glutathion peroxydase a diminue, alors que le taux d'ARNm oxydase de la NADPH a augmente significativement apres le traitement a la DEX. Ces resultats donnent a penser qu'un taux tres eleve de GC provoque une degradation de l'hippocampe en regulant les genes impliques dans la production des ROS. Mots-cles : glucocorticoide, hippocampe, neurotoxicite, culture organotypique de tranche d'hippocampe, especes reactives de l'oxygene, stress. [Traduit par la Redaction], Introduction The glucocorticoid (GC) steroid hormones released from the adrenal cortex are the principal effectors in the stress response (Sapolsky et al. 2000). Although short-term elevation of GCs can be [...]