ABSTRACT
Nicotine has been reported to induce oxidative stress both in vivo and in vitro. The present study was undertaken to examine the effect of nicotine on oxidative metabolism in skeletal muscle fibre types (Type I & Type II) of male albino rats. The animals were divided into two groups: Group-I (control), and Group-II (experimental). The latter received subcutaneous injections at a dose of 0.5 mg/ kg body weight (Experiment-I), 1 mg/kg body weight (Experiment-II), 5 days/week for a period of 8 weeks. The animals were sacrificed after 24 hours of the last treatment, and skeletal muscle fibres such as soleus (SOL), red vastus (RV) and white vastus (WV) were isolated and analyzed. The activity of lactate dehydrogenase (LDH) increased in nicotine-treated rats of both experiment-I, and experiment-II. Succinate dehydrogenase (SDH), isocitrate dehydrogenase (ICDH), malate dehydrogenase (MDH) and glucose-6-phosphate dehydrogenase (G-6-PDH) were decreased in soleus (SOL), red vastus (RV) and white vastus (WV) skeletal muscle fibres. These findings indicate nicotine-induced oxidative stress in the skeletal muscle fibres of male albino rats.
ABSTRACT
This study was conducted to know the influence of alcohol and aging on carbohydrate metabolic profiles in the kidney tissue of control and experimental male albino rats. Alcohol significantly decreased the levels of glucose, total proteins, total carbohydrates and increased free amino acids, pyruvate and lactate in the kidney tissue of both age groups of rats. Aging induced the elevation of the levels of glucose, total carbohydrates, free amino acids and lactate, while it decreased the total protein and pyruvate contents. This suggests rapid utilisation of carbohydrates and degradation of proteins to meet energy demands under alcoholic stress. Thus more alterations were observed in the carbohydrate metabolic profiles in kidney of both age groups of experimental rats.
ABSTRACT
Nicotine, a major constituent of tobacco, plays a critical role in smoking addiction. Nicotine has been reported to induce oxidative stress by producing Reactive Oxygen Species (ROS). The present study was undertaken to examine the effects of nicotine on the antioxidant defense systems in the skeletal muscle fibre types (Type I, Type II) of albino rats. The animals were divided into three groups of six animals each, i.e., control, experimental-1 and 2. The animals received subcutaneous injection of nicotine in physiological saline at a dose of 0.5 mg/kg (Exptl. 1), and 1 mg/kg (Exptl. 2), 5 days a week, for 8 weeks. The animals were sacrificed at 20 hrs after the last treatment, and the following muscle fibres were isolated and analyzed - soleus (Type I), red vastus, and white vastus (Type II). Nicotine was found to significantly deplete the rat muscle fibres GSH (glutathione) content, and the activity of GST (glutathione-s-transferase) and G-6-PD (glucose-6-phosphate dehydrogenase). This indicates that nicotine induces oxidative injury in the muscle fibres of rat.
ABSTRACT
One of the most widely used active ingredients in the world (for pest control) is deltamethrin, a synthetic pyrethroid. Deltamethrin is popular not only because of its effectiveness, but also for characteristics that allow the insecticide to work efficiently at low doses. Deltamethrin is a Type-II pyrethroid compound that is however highly toxic to fish, while being less toxic to birds and mammals. In the present study, Channa punctatus was used as an animal model to determine the toxicity of deltamethrin. Males weighing 10 ± 2g and females weighing 12 ± 2g were divided into groups of ten each and were exposed to different concentrations of deltamethrin ranging from 0.02 ppm to 0.2 ppm, for five exposure periods, i.e., 1, 7, 15, 20 and 30 days. The acetylcholinesterase (AChE) activity and actylcholine (ACh) content were estimated. The levels of AChE activity rose at 24 h relative to control in all the organs, whereas the ACh content dipped. Thereafter, the levels of AChE activity progressively decreased through 7 days, and continued upto the 15th day, mirroring the steady increase in ACh. From 15th day onwards, the levels of AChE activity gradually increased, and approached that of the control at 30 day exposure, whereas the levels of ACh content displayed an opposite trend.
ABSTRACT
Exercise together with chronic ingestion of ethanol produces physiological and morphological alterations in skeletal muscle. The present study has been carried out to investigate the combined effect of exercise and ethanol ingestion on selected energy metabolic profiles of skeletal muscle fibres with reference to age induced changes. Wistar strain albino rats of two age groups (3 months & 18 months) were divided into four groups - Group I, sedentary control (SC); Group II, exercise (ExT) (30 min, speed of 23 m/min/day/5 days/week for a period of 8 weeks); Group III, ethanol treated (Et) (20% ethanol, 2 gm/kg body weight); Group IV, exercise trained + ethanol treated (ExT + Et) as mentioned in Groups II and III. The animals were sacrificed after 24 hours of the last treatment by cervical dislocation, and the skeletal muscle fibres of gastrocnemius (GN) and soleus (SOL) were isolated from the hind limbs, and selected energy metabolic profiles such as carbohydrates, glycogen, and free amino acids were estimated. The total carbohydrate content, glycogen and FAA are significantly elevated with ExT and also with combination treatment. However, the same parameters were decreased with ethanol intoxication in both skeletal muscle fibres when compared with sedentary control rats. The results suggest a beneficial role of exercise in preventing ethanol-induced toxicity.