Neuroprotective effect of quercetin in ectoenzymes and acetylcholinesterase activities in cerebral cortex synaptosomes of cadmium-exposed rats.

This study investigated the effect of quercetin on nucleoside triphosphate diphosphohydrolase (NTP-Dase), 50-nucleotidase, adenosine deaminase (ADA), and acetylcholinesterase (AChE) activities in synaptosomes from cerebral cortex of adult rats exposed to cadmium (Cd). Rats were exposed to Cd (2.5 mg/Kg) and quercetin (5, 25 or 50 mg/Kg) by gavage for 45 days. Rats were randomly divided into eight groups (n = 8-10): saline/ethanol, saline/Querc 5 mg/kg, saline/Querc 25 mg/kg, saline/Querc 50 mg/kg, Cd/ethanol, Cd/Querc 5 mg/kg, Cd/Querc 25 mg/kg, and Cd/Querc 50 mg/kg. Results demonstrated that AChE activity increased in the Cd/ethanol group when compared to saline/ethanol group. Treatment with quercetin prevented the increase in AChE activity when compared to Cd/ethanol group. Quercetin treatment prevented the cadmium-induced increase in NTPDase, 5-nucleotidase, and ADA activities in Cd/ethanol group when compared to saline/ethanol group. Our data showed that quercetin have a protector effect against Cd intoxication. This way, is a promising candidate among the flavonoids to be investigated as a therapeutic agent to attenuate neurological disorders associated with Cd intoxication.

Physical training prevents oxidative stress in L-NAME-induced hypertension rats.

The present study investigated the effects of a 6-week swimming training on blood pressure, nitric oxide (NO) levels and oxidative stress parameters such as protein and lipid oxidation, antioxidant enzyme activity and endogenous non-enzymatic antioxidant content in kidney and circulating fluids, as well as on serum biochemical parameters (cholesterol, triglycerides, urea and creatinine) from Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME)-induced hypertension treated rats. Animals were divided into four groups (n = 10): Control, Exercise, L-NAME and Exercise L-NAME. Results showed that exercise prevented a decrease in NO levels in hypertensive rats (P < 0·05). An increase in protein and lipid oxidation observed in the L-NAME-treated group was reverted by physical training in serum from the Exercise L-NAME group (P < 0·05). A decrease in the catalase (CAT) and superoxide dismutase (SOD) activities in the L-NAME group was observed when compared with normotensive groups (P < 0·05). In kidney, exercise significantly augmented the CAT and SOD activities in the Exercise L-NAME group when compared with the L-NAME group (P < 0·05). There was a decrease in the non-protein thiols (NPSH) levels in the L-NAME-treated group when compared with the normotensive groups (P < 0·05). In the Exercise L-NAME group, there was an increase in NPSH levels when compared with the L-NAME group (P < 0·05). The elevation in serum cholesterol, triglycerides, urea and creatinine levels observed in the L-NAME group were reverted to levels close to normal by exercise in the Exercise L-NAME group (P < 0·05). Exercise training had hypotensive effect, reducing blood pressure in the Exercise L-NAME group (P < 0·05). These findings suggest that physical training could have a protector effect against oxidative damage and renal injury caused by hypertension.

Vitamin E decreased the activity of acetylcholinesterase and level of lipid peroxidation in brain of rats exposed to aged and diluted sidestream smoke.

INTRODUCTION: The biological systems of both smoker and passive smoking suffer changes caused by toxic compounds from cigarette smoke such as inflammation, lipid peroxidation, and deficiency of vitamin E. The aim of the present study was to evaluate the effect of vitamin E on acetylcholinesterase (AChE) activity and the lipid peroxidation level in the brain of rats in the model of exposure to aged and diluted sidestream smoke (ADSS). METHODS: Adult male Wistar rats (200-300 g) were exposed to ADSS for 4 weeks and treated with vitamin E (50 mg/kg/day) loaded by gavage. In the first, second, third, and fourth weeks, animals were concomitantly exposed to the smoke of 1, 2, 3, and 4 cigarettes/day, respectively. The duration of each exposure was 15 min, daily. RESULTS: For rats exposed to ADSS, the AChE activity and lipid peroxidation level increased in the striatum, cerebral cortex, and cerebellum. In contrast, the activity of AChE and the level of lipid peroxidation decreased in the smoke group treated with vitamin E. CONCLUSIONS: The results suggest that the rats exposed to ADSS and treated with vitamin E significantly reduced the raised activity of AChE and level lipid peroxidation from the brain structures studied. The study, therefore, concludes that vitamin E could be considered as a therapeutic agent in this type of exposure.

Swimming training prevents alterations in acetylcholinesterase and butyrylcholinesterase activities in hypertensive rats.

BACKGROUND: Cholinergic enzyme activities are altered in hypertension, reflecting a low-grade inflammation. Regular physical exercise exerts anti-inflammatory effects and has been described as a coadjutant in the treatment of hypertension. In this study, we investigated the effect of 6 weeks of swimming training on cholinergic enzyme activities (acetylcholinesterase and butyrylcholinesterase) in Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME)-induced hypertensive rats. METHODS: The rats were divided into 4 groups: control (n = 10), exercise (n = 10), L-NAME (n = 10), and exercise L-NAME (n = 10). The animals were trained 5 times per week in an adapted swimming system for 60 minutes with a gradual increase of the workload up to 5% of animal's body weight. Enzyme activities were measured spectrophotometrically in lymphocytes, whole blood, and serum. RESULTS: A significant rise in acetylcholinesterase activity was observed in lymphocytes and whole blood as well as in serum butyrylcholinesterase activity in the L-NAME group when compared with the other groups (P < 0.05), and the increase in cholinesterase activities was positively correlated with the rise in blood pressure (r = 0.5721, r = 0.6121, and r = 0.5811, respectively). Swimming training was efficient in preventing these alterations in the exercise L-NAME group, which displayed values similar to those of the control group. Exercise training demonstrated a significant hypotensive effect in hypertensive rats. CONCLUSIONS: Exercise training was shown to prevent increased cholinesterase related to inflammatory processes in hypertensive rats, providing a new insight about protective exercise mechanisms to avoid hypertension-related inflammation.

Nicotine alters the ectonucleotidases activities in lymphocytes: In vitro and in vivo studies.

The aim of the present study was to investigate the effects in vivo and in vitro of nicotine, an important immunosuppressive agent, on NTPDase and ADA activities in lymphocytes of adult rats. The following nicotine doses in vivo study were evaluated: 0.0, 0.25 and 1.0mg/kg/day injected subcutaneously in rats for 10days. The activity of the enzymes were significantly decreased with nicotine 0.25 and 1mg/kg which inhibited ATP (22%, 54%), ADP (44%, 30%) hydrolysis and adenosine (43%, 34%) deamination, respectively. The expression of the protein NTPDase in rat lymphocytes was decreased to nicotine 1mg/kg and the lymphocytes count was decreased in both nicotine doses studied. The purine levels measured in serum of the rats treated with nicotine 0.25mg/kg significantly increased to ATP (39%), ADP (39%) and adenosine (303%). The nicotine exposure marker was determinate by level of cotinine level which significantly increased in rats treated with nicotine 0.25 (39%) and 1mg/kg (131%) when compared to rats that received only saline. The second set of study was in vitro assay which the ATP-ADP-adenosine hydrolysis were decreased by nicotine concentrations 1mM (0% - 0% - 16%, respectively), 5mM (42% - 32% - 74%, respectively), 10mM (80% - 27% - 80%, respectively) and 50mM (96% - 49% - 98%, respectively) when compared with the control group. We suggest that alterations in the activities of these enzymes may contribute to the understanding of the mechanisms involved in the suppression of immune response caused by nicotine.