Oxidative Damage In Intestine Research Articles

Diverse role of gut microbiota on reduction of ascites and intestinal injury in malignant ascites effusion rats treated with Euphorbia kansui stir-fried with vinegar

Euphorbia kansui (EK) is the dried root of Euphorbia kansui S.L.Liou ex S.B.Ho. Clinically, processing with vinegar is for reducing toxicity of EK, and EK stir-fried with vinegar (VEK) is used to treat ascites and edema. VEK has been confirmed to reduce ascites by accelerating the promotion of intestinal contents. The study aimed to investigate whether gut microbiota could affect the expelling water retention effects and the intestinal oxidative damage of EK and VEK on malignant ascites effusion (MAE) rats. Pseudo-germ-free (PGF) MAE rats or probiotic intervented MAE rats were treated with EK/VEK. Related indicators such as serum, ascites, urine, feces, gastrointestinal tissues were analyzed, and the structure of the gut microbiota were also studied. The relationship between gut microbiota and the expelling water retention effects of EK/VEK where then further investigated. VEK reduce the volume of ascites by promoting urine and feces excretion, AQP8 protein and mRNA expression, when comparing with the MAE rats, also VEK could regulate the disordered gut microbiota in MAE rats. Mixed antibiotics could diminish VEK's expelling water retention effects in MAE rats, but increased oxidative damage in intestine. While existence of gut microbiota (especially probiotics) played an important role in the protection of intestines in VEK treated MAE rats. VEK had obvious pharmacological effect on MAE and could regulate gut microbiota, but gut microbiota was not a necessary condition for its pharmacological effects. The probiotics played a synergistic role with VEK in the effects of expelling water retention and intestinal protection.

Preventive effect of wheat germ oil on methotrexate – induced liver injury and oxidative intestinal damage in mice.

Methotrexate (MTX) is an anti-neoplastic drug that is widely used in the treatment of several diseases such as lymphoblastic leukemia, lymphoma, and autoimmune diseases, and has been concomitant with mild or severe liver and intestinal toxicity. One of the most attractive approaches to prevent toxicity of different organs involves the use of natural antioxidants. Thus, the present investigation was undertaken to study the possible protective effect of wheat germ oil (WGO) against single dose of methotrexate induced oxidative stress in hepatic and intestinal tissue. The oxidative stress was induced using single intraperitoneal injection of methotrexate (20 mg/kg body weight), while the protecting effect was investigated by oral administration of WGO (1400 mg/kg body weight), for six and three consecutive days before and after MTX injection respectively. MTX has revealed significant depletion of some oxidative biomarkers and an elevation in the activities of liver enzymes, Lactate dehydrogenase (LDH), intestinal malondialdehyde (MDA), lipid profile, and remarkable intestinal DNA damage, as well as abnormal architecture of mucosa. The present findings confirmed that WGO has significant preventive effect against liver injury and intestinal oxidative stress induced by MTX through improving the liver enzymes levels, enhancing the intestinal antioxidant defense status, reduction of lipid peroxidation level, and protection against different pathological changes. Taken together, it’s then recommended to give WGO to individuals who are treated with MTX, although more pharmacological and molecular assays are necessary to elucidate its protective mechanisms

Close association of intestinal autofluorescence with the formation of severe oxidative damage in intestine of nematodes chronically exposed to Al 2O 3-nanoparticle

In nematodes, acute exposure (24-h) to 8.1-30.6 mg/L Al(2)O(3)-nanoparticles (NPs) or Al(2)O(3) did not influence intestinal autofluorescence, whereas chronic exposure (10-d) to Al(2)O(3)-NPs at concentrations of 8.1-30.6 mg/L or Al(2)O(3) at concentrations of 23.1-30.6 mg/L induced significant increases of intestinal lipofuscin accumulation, and formation of severe stress response and oxidative damage in intestines. Moreover, significant differences of intestinal autofluorescence, stress response and oxidative damage in intestines of Al(2)O(3)-NPs exposed nematodes from those in Al(2)O(3) exposed nematodes were detected at examined concentrations. Oxidative damage in intestine was significantly correlated with intestinal autofluorescence in exposed nematodes, and oxidative damage in intestine was more closely associated with intestinal autofluorescence in nematodes exposed to Al(2)O(3)-NPs than exposed to Al(2)O(3). Thus, chronic exposure to Al(2)O(3)-NPs may cause adverse effects on intestinal lipofuscin accumulation by inducing the formation of more severe oxidative stress in intestines than exposure to Al(2)O(3) in nematodes.

Melatonin ameliorates oxidative intestinal damage induced by acute intraabdominal compartment syndrome in the rats

Melatonin ameliorates oxidative intestinal damage induced by acute intraabdominal compartment syndrome in the rats

Intestinal, hepatic and renal production of thiobarbituric acid reactive substances and myeloperoxidase activity after temporary aortic occlusion and reperfusion

Ischemia induced oxygen free radical damage was formerly attributed only to xanthine oxidase in intestine, liver, kidney and heart. A reevaluation indicated neutrophils as one of the major sources of postischemic oxidative tissue damage, chiefly in the intestine. Our data, obtained from the same occlusion time period for intestine, liver and kidney, showed a certain oxidative damage in intestine and kidney already during ischemia, expressed by an increase of thiobarbituric acid reactive substances (TBARS), whereas the liver sustained damage of this kind only during reperfusion. Oxidative stress was expressed by a comparison of the increase of TBARS, though this test is not a measure of a specific product of lipid peroxidation, but rather comprises several breakdown products of free radical damage. Myeloperoxidase as measure of neutrophil stimulation increased in the intestine and liver. The kidney sustained damage without an increase of myeloperoxidase activity, but showed a similar pattern of increase of TBARS as in the intestine. Our data suggest a major role of neutrophils in intestinal ischemia induced damage, where neutrophils can effect initiation and propagation. In the liver neutrophils may play a minor role concerning propagation, but they may act as an important initiating mechanism. Hepatic tissue shows a high ischemic tolerance, which is demonstrated by a missing increase of TBARS in spite of a certain increase of myeloperoxidase activity during ischemia. This can be interpreted by the high capacity of antioxidative mechanisms of liver tissue and the ability of a higher oxygen extraction ratio under nearly ischemic conditions. In the kidney there appears a smaller contribution of neutrophils. The similar pattern of increase of TBARS in kidney and intestine demonstrates a comparable low ischemic tolerance of these two tissues, whereas different initiating and propagating systems may occur.