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EN
The aim of the study was to evaluate the influence of vitamin E administered intraperitoneally on the prevention of peritoneal adhesion formation in rats on the basis of macroscopic and microscopic assessment of the adhesions.Material and methods. Experimental studies were performed on 50 Sprague-Dawley male rats, which were randomly divided into 5 groups, 10 rats in a group. Experimental group I (EI) included 10 rats which had peritoneal adhesions provoked by scraping of the wall of cecum and parietal peritoneum followed by intraperitoneal administration of vitamin E in the dose of 100 mg/kg body weight. Experimental group II (EII) included 10 rats which had peritoneal adhesions provoked by surgery, without administration of vitamin E. Control Group I (CI) included 10 rats which had the abdominal cavity opened without provoking peritoneal adhesions, and vitamin E was administered. Control Group II (CII) included 10 rats which had peritoneal adhesions provoked by surgery, and then lipid based solution was administered intraperitoneally. Control Group III (CIII) included 10 rats which had the abdominal cavity only opened and closed.Groups EI, CI and CII were the subject of the drugs intraperitoneal re-injection in first, second and third day after surgery. The animals were killed during the 8th postoperative day. Macroscopic examination of peritoneal adhesions using the classification reported by Nair was performed and samples for microscopic examination were excised.Results. In group EI peritoneal adhesions were formed in 60% rats (40% weak and 20% solid). In group EII peritoneal adhesions were found in all animals (30% weak and 70% solid). Reduction of the inflammatory response and less severe fibrosis were observed in animals with intraperitoneal administration of vitamin E.Conclusion. In the study, vitamin E administered intraperitoneally to rats decreased the intensity and extensiveness of peritoneal adhesions, which was confirmed by macroscopic and microscopic examinations.
EN
The liver as a vital body organ is adversely affected by hazardous chemicals and drugs. Paracetamol widely used as analgesic and antipyretic drug produces severe hepatotoxicity at high doses. Present study was designed to investigate the hepatoprotective activity of Polygonum perfoliatum L. used on folklore basis. Aqueous methanolic extract of the plant was prepared. Preliminary phytochemical and HPLC analyses were carried out to identify and quantify chemical constituents respectively. For hepatoprotective activity, Wistar rats were divided into six groups as normal control, standard (silymarin) control, negative control and extract treated groups i.e., 125, 250 and 500 mg/kg/day per oral. Paracetamol was administered orally, following seven days of previously stated therapy. Biochemical parameters of hepatotoxicity such as serum glutamic pyruvate transaminase (SGPT), serum glutamic oxaloacetate transaminase (SGOT), alkaline phosphatase (ALP) and total bilirubin were measured in all groups. Histopathological evaluation of liver was also carried out. Benzoic acid, chlorogenic acid, gallic acid, m-coumaric acid, quercetin and vitamin E were detected in the plant extract through HPLC. The hepatoprotective effect of 500 mg/kg/day therapy was more pronounced than 125 and 250 mg/kg dose. However, the effect of plant extract was less pronounced than standard silymarin therapy. It can be concluded that the plant extract possessed significant hepatoprotective activity that may be attributed to quercetin, benzoic acid, gallic acid and vitamin E present in it.
5
75%
|
2001
|
vol. 48
|
issue 1
283-285
EN
Activities of superoxide dismutase, catalase and glutathione peroxidase in erythrocytes of cystic fibrosis children were studied in order to estimate the severity of their deficiency. Our results point to increased susceptibility of erythrocytes of cystic fibrosis subjects to oxidative injury and indicate that the antioxidant status of patients should be carefully monitored.
|
2003
|
vol. 50
|
issue 1
205-210
EN
Alloxan can generate diabetes in experimental animals and its action can be associated with the production of free radicals. It is therefore important to check how different substances often referred to as free radical scavengers may interact with alloxan, especially that some of these substance may show both pro- and antioxidant activities. Using the alkaline comet assay we showed that alloxan at concentrations 0.01-50 μM induced DNA damage in normal human lymphocytes in a dose-dependent manner. Treated cells were able to recover within a 120-min incubation. Vitamins C and E at 10 and 50 μM diminished the extent of DNA damage induced by 50 μM alloxan. Pre-treatment of the lymphocytes with a nitrone spin trap, α-(4-pyridil-1-oxide)- N-t-butylnitrone (POBN) or ebselen (2-phenyl-1,2-benzisoselenazol-3(2H)-one), which mimics glutathione peroxides, reduced the alloxan-evoked DNA damage. The cells exposed to alloxan and treated with formamidopyrimidine-DNA glycosylase (Fpg) and 3-methyladenine-DNA glycosylase II (AlkA), enzymes recognizing oxidized and alkylated bases, respectively, displayed greater extent of DNA damage than those not treated with these enzymes. The results confirmed that free radicals are involved in the formation of DNA lesions induced by alloxan. The results also suggest that alloxan can generate oxidized DNA bases with a preference for purines and contribute to their alkylation.
EN
Vitamins D, C, E and A, which belong to antioxidants, exhibit anticancer activity. The mechanism of vitamin D antitumor activity involves the inhibition of cell proliferation, stimulation of apoptosis, inhibition of angiogenesis and an increased activity of metalloproteinases in the extracellular matrix. Vitamin D prevents the development and progression of breast cancer; its lower levels in the serum of premenopausal women are linked to the development of triple negative cancer (E-, PR-, HER2-). Cohort studies on the effects of VDR (vitamin D receptor) polymorphisms and studies related to vitamin D supplementation in postmenopausal women in the context of reduced risk of breast cancer are controversial. Vitamin D exerts a protective effect against ovarian and endometrial cancer. Vitamin C protects cells against the formation of mutagenic nitro compounds, enhances the immune system by promoting the activity of NK, T and B cells. Vitamin C supplementation improves treatment outcomes in disseminated breast cancer; the vitamin acts synergistically with cisplatin, it increases paclitaxel and doxorubicin cytotoxicity and abolishes toxic effects of tamoxifen. Vitamin C combined with chemotherapy in ovarian cancer prolongs patient’s survival. It increases sensitivity to cisplatin. Vitamin E exerts anticancer effects via multiple pathways. Its increased administration reduces the risk of breast cancer and ovarian cancer. The reduction in the incidence of endometrial cancer remains controversial. Vitamin A also exerts antioxidant effects. The compound reduces the incidence of DNA damage in cells exposed to hydrogen peroxide and protects cell organelles (including mitochondria) against the negative impact of lipid peroxidation. It reduces the risk of multiple tumors, including breast and cervical cancer.
PL
Witamina D oraz witaminy C, E i A, należące do antyoksydantów, wykazują aktywność przeciwnowotworową. Mechanizm działania witaminy D obejmuje hamowanie proliferacji komórkowej, stymulację apoptozy, hamowanie angiogenezy i zwiększanie aktywności metaloproteinaz macierzy pozakomórkowej. Witamina D zapobiega rozwojowi raka piersi i progresji choroby; niższe jej stężenia w surowicy kobiet przed menopauzą wiążą się z rozwojem raków potrójnie negatywnych (E-, PR-, HER2-). Badania kohortowe dotyczące wpływu polimorfizmów genu VRD (vitamin D receptor) oraz badania nad suplementacją witaminy D po menopauzie w kontekście redukcji rozwoju raka piersi są kontrowersyjne. Witamina D ma protekcyjny wpływ w przypadku raka jajnika i endometrium. Witamina C chroni komórki przed mutagennym tworzeniem nitrozwiązków, wzmacnia funkcjonowanie układu immunologicznego przez wzrost aktywności komórek NK oraz limfocytów T i B. Stosowanie witaminy C poprawia wyniki leczenia rozsianego raka piersi; działa ona synergistycznie z cisplatyną, zwiększa cytotoksyczność paklitakselu i doksorubicyny, znosi toksyczny wpływ tamoksyfenu. Witamina C w skojarzeniu z chemioterapią przyczynia się do dłuższego przeżycia pacjentek z rakiem jajnika i poprawia wrażliwość na stosowaną cisplatynę. Witamina E działa przeciwnowotworowo przez wiele ścieżek. Jej zwiększona podaż wiąże się ze spadkiem ryzyka wystąpienia raka piersi i raka jajnika. Obniżenie ryzyka zachorowania na raka endometrium jest kontrowersyjne. Witamina A także ma działanie antyoksydacyjne. Obniża częstość uszkodzeń DNA indukowanych nadtlenkiem wodoru i chroni organella komórkowe (w tym mitochondria) przed negatywnymi skutkami peroksydacji lipidów. Zmniejsza ryzyko rozwoju wielu nowotworów, w tym raka piersi i szyjki macicy.
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