Gluconeogenesis, glycolysis and glycogenolysis were studied in rat perfused liver following the infusion of various concentrations of diclofenac and aspirin, two non-steroidal anti-inflammatory drugs (NSAIDs). Glucose synthesis was measured in livers isolated from 48-h fasted rats perfused with Krebs-Henseleit bicarbonate buffer containing L-lactate (2 mM) and pyruvate (0.1 mM) as precursors. Both diclofenac (0.01-0.1 mM) and aspirin (1-10 mM) had an inhibitory effect on gluconeogenesis (GNG). The inhibition was dose-dependent and reversible. For the estimation of glycogenolysis and glycolysis, the rates of glucose release and of lactate and pyruvate production were measured in livers of well-fed rats perfused with substrate-free buffer. Infusion of diclofenac (0.1 mM) or aspirin (5 mM) strongly stimulated glycogenolysis and glycolysis (GGL/GL). In general, an increased oxygen consumption by the liver tissue was also noted in both types of experiments, as deduced from the continuous monitoring of oxygen concentration changes in the effluent. Such a pattern of response can be attributed to the uncoupling effects of the two drugs on oxidative phosphorylation. Measurements of respiration rates and membrane potential in isolated liver mitochondria submitted to various concentrations of diclofenac and aspirin confirms this assumption. Thus, 0.01 to 0.2 mM diclofenac stimulates state-4 respiration and slightly inhibits state 3, decreasing the respiratory control ratio, while the membrane potential is decreased or collapsed (depending on the drug concentration). Similar effects are recorded for aspirin at higher concentrations (0.2-5 mM), even though state 3 is not affected in this case. Arguments are presented that the concentrations of the drugs used largely correspond to the pharmacological doses employed in antipyretic and anti-inflammatory treatments. Therefore, a greater consideration should be given to the uncoupling effect, at least from the toxicological viewpoint.
Objective:Energy drinks (EDs) target young and active individuals and they are being marketed as enhancers of energy, concentration, and physical and cognitive performance. Their long-term consumption raises serious health concerns related to cardiovascular events. Here we investigate the effects of long-term Red Bull® consumption and its combination with alcohol on certain biochemical parameters and the ultrastructure of the myocardium.Methods:Male Wistar rats were categorized into four groups and given different treatments via oral administration. The Control (C) group received tap water, the Red Bull (RB) group received 1.5 ml/100 g body weight of Red Bull, the ethanol group (E) received 0.486 mg/100 g body weight of ethanol, and the Red Bull and ethanol (RBE) received a combination of the two beverages for 30 days. In the last 6 days of the experiment, the animals were tested for their physical performance by conducting a weight-loaded forced swim test. Immediately after swimming exhaustion, the animals were sacrificed under anesthesia and samples of the heart muscle were harvested for ultrastructural and biochemical analyses.Results:Our results showed a significant increase in the heart glucose and glycogen concentrations in the RB and RBE groups. Total cholesterol concentration significantly decreased in the RBE and RB groups. Total protein concentration and ALT and AST activities increased in all groups. The biochemical changes were accompanied by ultrastructural alterations.Conclusion:Based on these results, we recommend that athletes and active persons should avoid the long-term consumption of the Red Bull ED and, particularly, its combination with alcohol.
EGF protects the liver against both alcohol-induced liver damage and liver sensitization to bacterial LPS through down-regulation of apoptosis.
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