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The authors studied the effect of a single injection of dibunol in a dose of 120 mg/kg on lipid peroxidation (LPO) and alpha-tocopherol (TP) level in the heart muscle in acute blood loss. The LPO products and alpha-tocopherol level were determined simultaneously in a heart homogenate 2 hours after
The accumulation of lipid peroxidation (LP) products and decrease of alpha-tocopherol (TP) content were demonstrable in the heart, lungs, kidneys and liver after acute blood loss. Injection of TP acetate inhibited LP and raised the content of endogenous TP in the heart, lungs and liver. The
Experiments on linear male rats were made to study the pathophysiological mechanism of the synthetic antioxidant dibunol on the levels of primary and end products of lipid peroxidation (LPO) and of alpha-tocopherol (TP) in the lungs in acute hemorrhage. Dibunol in a dose of 120 mg/kg injected 5 min
Forty four babies, of less than 32 weeks' gestation, were either randomly given 25 mg/kg vitamin E (DL-alpha-tocopherol acetate) intramuscularly after birth (day 0) and on days 1, 2, and 3 or served as controls. Frequent real time ultrasound examinations of the brain were made in each baby during
When male Sprague-Dawley rats were administered d-alpha-tocopherol and butylated hydroxytoluene in the diet or intraperitoneally for 7 days, prolongations of prothrombin time and partial thromboplastin time were observed in those given both chemicals by both routes in a dose-dependent manner.
Alpha-tocopherol (vitamin E) may play a role in the treatment of arterial thromboembolic disease, possibly by inhibiting platelet aggregation. Thus far, no clinical evidence exists for this effect. The objective of this study was to assess the effect of alpha-tocopherol supplementation on gingival
The effect of single administration of alpha-tocopherol at a dose of 50 mg/kg on lipid peroxidation, content of alpha-tocopherol in liver tissue and on the activities of some enzymes in rat serum was studied under conditions of acute blood loss. The rate of lipid peroxidation in liver tissue and
Up to 41% of intracerebral hemorrhages (ICH) are considered cryptogenic despite a thorough investigation to determine etiology. Certain over-the-counter supplements may increase proclivity to bleeding, and we hypothesize that specifically vitamin E may have an association with ICH and Effect of little doses of sodium selenite combined with alpha-tocopherol on microcirculation was studied in experimental bloodletting in dogs. It was established that more rapid recovery, as compared to control, of blood flow in the visceral basin and more rapid elevation of arterial blood pressure
A randomized, double-blind study to determine the effect of intramuscular vitamin E on mortality and intracranial hemorrhage (ICH) was performed. One hundred forty-nine neonates with birth weights less than or equal to 1000 g and less than or equal to 24 hours of age were grouped by weight (501 to
Background and objectives: Few studies have assessed the possible interaction between and impact of IL-6 variants and serum α-tocopherol levels on periodontal condition in older individuals. Here, we assessed the relationship between IL-6
Despite evidence that Helicobacter pylori (H. pylori) infection is closely associated with stress in gastric ulcer patients, the underlying mechanism why ulcer recurrence after stress is augmented especially in patients with H. pylori remains unknown. In this study, we found that oxidative stress
Effects of chronic (14 day) pretreatment of timed-release of alpha-tocopherol (approximately 1.25-5 mg/day) on alcohol-induced venular cerebrovasospasm, microvessel rupture and micro-hemorrhaging was studied by direct, quantitative in-vivo high-resolution TV microscopy of the intact rat brain. Sham
Vitamin E appears to be a safe, simple, and inexpensive means of reducing the number of postoperative capsular contractures following breast augmentation. The synthetic form of vitamin E (alpha-tocopherol) is recommended to avoid nausea or skin eruptions in patients with oily skin, which are
The nephrotoxic actions of aluminium (Al) arise from its accumulation in the kidneys, with the resultant degeneration of the renal tubular cells. It has been suggested that Al generates reactive oxygen species that cause the oxidative deterioration of cellular lipids, proteins, and DNA. To test this