Potential preventive and therapeutic effects of glutathione supplementation in experimental colitis

The aim of this study was to assess the potential preventive and therapeutic effects of glurathione [GSH] on inflammatory bowel diseases [IBD] and to evaluate the use of fecal calprotectin [FC] and fecal lactoferrjn [Lf] as a non-invasive diagnostic marker of IBD. Forty albino rats were divided into four groups; group I: control group; group II: acetic acid induced colitis group, group III: after colitis induction, rats were treated with glutathione for one week [50 mg/kg, i.p.] and group IV: before the induction of colitis, rats were given a preventive dose of glutathione [200 mg/kg, i.p]. At the end of experimental period, rats were sacrificed, fecal calprotectin and lactoferrin were assessed in the different groups, the level of antioxidants in the intestine was evaluated and the severity of inflammation was histopathologically scored. Intestinal glutathione level was decreased significantly after colitis induction, however, it was significantly high in the prevention group. There was significant reduction in the antioxidant enzymes after colitis induction. However, glutathione prevention was associated with higher antioxidant enzymes compared to treatment. Various histopathological changes as inflammation, ulceration and dysplasia were detected after colitis induction and in rats treated with glutathione, however, rats supplemented with glutathione as prevention showed no ulceration and mild inflammation. In addition, colitis induction was associated with significant increase in the colonic level of FC and Lf which was significantly reduced with glutathione prevention. Glutathione prevention appeared to be beneficial for the acute stage of IBD than glurathione treatment. Moreover, intestinal antioxidant enzymes were correlated negatively with FC level. FC and Lf can be used as non-invasive and simple marker for diagnosis of IBD

Physiologic effects of maternal separation on rat brain neurochemistry: comparative study

Exposure to maternal separation in early life is associated with alteration in the neuroendocrine and neurotransmitter system which may be associated with risk of psychiatric disorders development at adulthood. The aim of this study was to [i] assess levels of monoamines [dopamine, nor-epinephrine, epinephrine and serotonin] in rat pup's brain following repeated maternal separation [RMS] and maternal deprivation [MD]. [ii] Assess brain corticosterone and oxytocin level following both RMS and MD. This study was carried out on 50 male rat pups divided into 3 experimental groups; Group I: 20 rats subjected to 3 h of repeated maternal separation for 14 days; Group II: 20 rats subjected to 24 h of maternal deprivation; Group III: 10 rats served as control group. At the end of the experimental period, all rats were sacrificed and their brains were rapidly removed and dissected for estimation of monoamines, corticosterone and oxytocin. Brain corticosterone level showed marked increase after both separation procedures, however, MD was associated with marked increase. RMS was associated with higher level of epinephrine, norepinephrine, dopamine and serotonin. Dopamine and serotonin levels however, were reduced after MD. Oxytocin level showed marked reduction after MD and RMS. The current work provided some neurobiological evidence supporting the determinant role of mother-infant relationship in the development of psychopathology. Maternal separation leads to profound alterations in the central neurotransmitter system and therefore is associated with increased risk of psychiatric disorders as depression and anxiety. Moreover, maternal separation has impact on the corticosterone and oxytocin release in the brain. Different separation procedures however, can influence the consequences of MS

Influence of the antioxidant drug [antox] on experimental giardiasis and microsporidiosis

The effect of antioxidant [Antox] on Giardia lamblia and Microsporidium sp. in rats and mice respectively was studied. Pa-rasitologic effect was assessed by the mean parasitic count in infected animals' stool treated and non-treated, and infection intensity in stained section. Biochemical by measuring activities of lactate dehydrogenase [LDH], superoxide dismutase [SOD], malondialdehyde [MDA], myeloperoxidase [MPO] levels and cytokine induced neutrophil chemoattractant-1 [CINC-1] in intestinal homogenates in these animals as shown by cell injury, lipid peroxidation and neutrophil infiltrations. The present results showed that Antox significantly exacerbated G. lamblia and Microsporidium sp. This was manifested by a significant increase in number of G. lamblia cysts and trophozoites in stool and intestinal sections of treated infected rats. Also, microsporidian spores were significantly higher in stool of treated infected mice and infection intensity increased in the intestinal sections. The biochemical study showed a significantly higher degree of cell injury, lipid peroxidation and intestinal neutrophils accumulation in non-treated infected animals whether with G. lamblia or microsporidia. The changes reduced after treatment in giard-iasis but none in microsporidiosis. The results were tabulated photographed, and critically discussed

Fecal calprotectin, novel index for assessing the pathophysiological mechanisms of inflammatory bowel disease in rats treated by glutathione

In this study, the role of fecal calprotectin [FC] as a recent non-invasive diagnostic aid of inflammatory bowel disease [IBD] was evaluated and the effect of glutathione as a preventive and therapeutic factor in acetic acid induced colitis has been studied. Forty albino rats were divided into four groups; group I: acetic acid induced colitis group. Group II: before the induction of colitis, rats were given a preventive dose of glutathione [200 mg/kg, i.p]. Group III: after colitis induction rats were treated with glutathione for one week [50 mg/kg,i.p.]. Group IV: control group. At the end of experimental period, rats were sacrificed and fecal caiprotectin was assessed in the different groups, the level of antioxidant system in the intestine was evaluated and the severity of inflammation was histopathologically scored. Colitis induction was associated with significant increase in the colonic level of FC, which was significantly reduced with glutathione prevention. Glutathione level was decreased significantly in the intestine after colitis induction, however, it was significantly high in the prevention 'group. There was significant reduction in the antioxidant enzyme system after colitis induction. However, glutathione prevention was associated with higher antioxidant enzymes compared to treatment. Various histopathological changes as inflammation, ulceration and dysplasia were detected after colitis induction, group III, however, showed no ulceration and mild inflammation. Fecal caiprotectin can be used as a non-invasive and early marker for IBD. Glutathione prevention appeared to be beneficial for the acute stage of IBD than glutathione treatment. Moreover, intestinal antioxidant enzymes were correlated negatively with FC level

Study of oxidative stress, anti-oxidant status and their relation to apoptosis in acute lymphoblastic leukemia

Acute lymphoblastic leukemias [ALL] are the most common forms of childhood cancer. The exact etiology of acute leukemia is multifactorial. Oxidative stress and apoptosis are among the most important in the pathogenesis of ALL. The aim of the present study is to study the status of oxidative stress [oxygen free radicals and the anti-oxidant activity] in children with acute lymphoblastic leukemia [ALL] and its relation to apoptotic pathway by studying Fas receptor/Fas ligand [FasL] and Bcl-2. The study is conducted on 20 children suffering from acute lymphoblastic leukemia, and 10 age and sex-matched healthy children as a control group. Estimation of plasma levels of albumin, uric acid and bilirubin [as examples of anti-oxidants], anti-oxidant enzyme superoxide dismutase [SOD], Malonyldialdehyde [MDA] which reflects the extent of oxidative stress is performed. Also soluble Fas-L and Bcl-2 are assayed [to reflect apoptosis]. Levels of malonyldialdehyde are found to be elevated and SOD activity is reduced which reflects oxidative stress in ALL patients. Also ALL patients showed elevated levels of sFasL and Bcl-2. From the present study, it can be concluded that patients suffering from acute lymphoblastic leukemia are subjected to greater oxidative stress than normal children. This oxidative stress may be due to their greater exposure to oxygen free radicals or due to defective anti-oxidant defense mechanisms in these patients. It is also found that ALL is associated with defect in apoptosis as evidenced by increased expression of Bcl-2 [anti-apoptotic] and increased sFas-L, which opposes the Fas/CD95 pathway [pro-apoptotic]. This anti-apoptosis may be induced by increased oxidative stress in these ALL patients