Exercise increases markers of spermatogenesis in rats selectively bred for low running capacity

The oxidative stress effect of exercise training on testis function is under debate. In the present study we used a unique rat model system developed by artificial selection for low and high intrinsic running capacity (LCR and HCR, respectively) to evaluate the effects of exercise training on apoptosis and spermatogenesis in testis. Twenty-four 13-month-old male rats were assigned to four groups: control LCR (LCR-C), trained LCR (LCR-T), control HCR (HCR-C), and trained HCR (HCR-T). Ten key proteins connecting aerobic exercise capacity and general testes function were assessed, including those that are vital for mitochondrial biogenesis. The VO2 max of LCR-C group was about 30% lower than that of HCR-C rats, and the SIRT1 levels were also significantly lower than HCR-C. Twelve weeks of training significantly increased maximal oxygen consumption in LCR by nearly 40% whereas HCR remained unchanged. LCR-T had significantly higher levels of peroxisome proliferator-activated receptor-gamma coactivator-1 (PGC-1alpha), decreased levels of reactive oxygen species and increased acetylated p53 compared to LCR-C, while training produced no significant changes for these measures in HCR rats. BAX and Blc-2 were not different among all four groups. The levels of outer dense fibers -1 (Odf-1), a marker of spermatogenesis, increased in LCR-T rats, but decreased in HCR-TR rats. Moreover, exercise training increased the levels of lactate dehydrogenase C (LDHC) only in LCR rats. These data suggest that rats with low inborn exercise capacity can increase whole body oxygen consumption and running exercise capacity with endurance training and, in turn, increase spermatogenesis function via reduction in ROS and heightened activity of p53 in testes

Novel features of the rat model of inflammatory bowel disease based on 2,4,6-trinitrobenzenesulfonic acidinduced acute colitis

The 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced acute inflammatory bowel disease (IBD) model in the rat is discussed, focusing on the details of the TNBS instillation and highlighting the advantages and limitations of this model. For determination of the time-dependent action of 50% ethanol and different doses of TNBS, male Wistar rats were treated with 50% ethanol or 10 mg or 30 mg of TNBS dissolved in 50% ethanol. The TNBS-induced inflammation peaked 48-72 h after installation and the colitis caused by 30 mg of TNBS was more severe than that caused by 10 mg of TNBS. To test the effectiveness of sulfasalazine (SASP), male rats were treated with 10 mg of TNBS or with 10 mg of TNBS and SASP, and 72 h later the extent of mucosal damage was determined. Orally administered 50 mg/kg/day SASP proved to reduce the TNBS-induced colonic inflammation in rats significantly. The TNBS-induced colitis model facilitates a better understanding of the immunopathological mechanisms of IBD. Optimization of the dose of TNBS and oral SASP as positive control in TNBS-induced colitis in rats furnishes an appropriate test system for new anti-IBD drugs

Új HPLC eljárás az alfa-amiláz aktivitás és gátlás mérésére

The control of the hyperglycemia is crucial in the treatment of type II diabetes and other metabolic syndromes. In these situations, the α-amylases could play an important role in the increasing of the blood glucose level due the breakdown of the polysaccharides. The αamylases are the first enzymes, which take a part in the process of the releasing glucose monomers from complex polysaccharides. Therefore, the investigations of both α-amylase activities and the quantity of their inhibition are important on the field of anti-diabetic drug research. Our presented research was aimed to develop a new HPLC based method for the measurement of reaction product of α-amylase reaction using specially synthetized, pnitrophenyl-labelled maltooligomer substrate. After the enzyme reaction, three product was detectable possessing the chromophore-group during the reversed-phase separation. One of them was selected to follow the enzyme kinetic of the human salivary amylase applying linear regression on the area data acquired at different time points of the reaction. Furthermore, due to the specific substrate measuring only the α-amylase activity, our method could be used successfully also for the accurate measurement in the inhibition studies

Sexual dimorphism of cardiovascular ischemia susceptibility is mediated by heme oxygenase

We investigated the gender differences in heme-oxygenase (HO) enzyme, which produces endogenous vascular protective carbon monoxide (CO). We studied (1) the activity and expression of HO enzymes in the left ventricle (LV) and aorta, (2) basal increase in basal blood pressure provoked by arginine vasopressine (AVP) in vivo, (3) the heart perfusion induced by AVP, (4) the ST segment depression provoked by adrenaline and 30 seconds later phentolamine, and (5) the aorta ring contraction induced by AVP in female and male Wistar rats. We found that HO activity and the expression of HO-1 and HO-2 were increased in female rat aorta and LV. We demonstrated that the basal blood pressure and administration of AVP provoked blood pressure response are increased in the males; the female myocardium was less sensitive towards angina. Both differences could be aggravated by the inhibition of HO. The aorta rings were more susceptible towards vasoconstriction by AVP in males; isolated heart perfusion decrease was higher in males. The HO inhibition aggravated the heart perfusion in both sexes. In conclusion, the increased HO activity and expression in females might play a role in the sexual dimorphism of cardiovascular ischemia susceptibility during the reproductive age. © 2013 Anikó Pósa et al

Nitrát tolerancia a szívizomban = Nitrate tolerance in the myocardium

Nagy dózisú nitroglicerin ismételt alkalmazásával vaszkuláris nitrát toleranciát váltottunk ki kísérleti állatokban. Kimutattuk hogy vaszkuláris nitrát toleranciában a szív és az aorta génexpressziós profilja eltérően változik. A szívizom génexpressziós változását egyéb szisztémás metabolikus állapotokban (metabolikus szindróma) is leírtuk. Kimutattuk, hogy az iszkémiás posztkondícionálás infarktus méretet csökkentő hatása jelentősen mérséklődik vaszkuláris nitrát tolerancia fennállása esetén. Továbbá azt tapasztaltuk, hogy ez a jelenség független a túlélő kinázok aktiválódásától. Kísérletes urémiában viszont a prekondícionálás kardioprotektív hatása megtartott marad. Izolált perfundált szívekben kimutattuk, hogy mind a koronária lekötés előtt, mind pedig a reperfúzió előtt megkezdett nitroglicerin perfúzió csökkenti a kialakuló infarktus méretét. Azonban a nitroglicerinnek ez a kardioprotektív hatása vaszkuláris nitrát tolerancia fennállása esetén nem volt megfigyelhető. Igazoltuk, hogy a NO-donor SNAP védi a szimulált iszkémia/reoxigenizációnak kitett primer szívizomsejt tenyészeteket a sejtelhalástól, valószínűleg részben a cGMP-PKG jelátviteli útvonal aktiválása révén. Továbbá kimutattuk, hogy a reperfúzió kezdetén alkalmazott szakaszos nagyfrekvenciás ingerléssel is kiváltható posztkondícionáló hatás a szívben. | We have induced vascular nitrate tolerance in rats by repeated administration of high dose nitroglycerin. We have found that the gene expression profile of the heart and the aorta was differentially altered in response to the development of vascular nitrate tolerance. Alterations in cardiac gene expression were shown in other systemic metabolic conditions (i.e. metabolic syndrome) as well. We have shown that the infarct size limiting effect of ischemic postconditioning is attenuated in the state of vascular nitrate tolerance. Moreover, we have found that this phenomenon is independent of survival kinase activation. Experimental uremia. however, did not lead to the loss of ischemic preconditioning. We have demonstrated in ex vivo hearts that nitroglycerin perfusion decreased infarct size when started before coronary occlusion and also when only started before reperfusion. This cardioprotective effect of nitroglycerin was diminished in the state of vascular nitrate tolerance. We have shown that the NO-donor molecule SNAP is able to protect primary cardiomyocyte cultures against simulated ischemia/reperfusion at least in part via activation of cGMP-PKG signaling. We have found that a postconditioning effect can be induced by applying short periods of ventricular overdrive pacing at the onset of reperfusion

The Effects of Exercise Training and High Triglyceride Diet in an Estrogen Depleted Rat Model

Cardiovascular morbidity and mortality of premenopausal women are significantly lower compared to men of similar age. However, this protective effect evidently decreases after the onset of menopause. We hypothesized that physical exercise could be a potential therapeutic strategy to improve inflammatory processes and cardiovascular antioxidant homeostasis, which can be affected by the loss of estrogen and the adverse environmental factors, such as overnutrition. Ovariectomized (OVX, n= 40) and sham-operated (SO, n= 40) female Wistar rats were randomized to exercising (R) and non-exercising (NR) groups. Feeding parameters were chosen to make a standard chow (CTRL) or a high triglyceride diet (HT) for 12 weeks. Aortic and cardiac heme oxygenase (HO) activity and HO-1 concentrations significantly decreased in all of the NR OVX and SO HT groups. However, the 12-week physical exercise was found to improve HO-1 values. Plasma IL-6 concentrations were higher in the NR OVX animals and rats fed HT diet compared to SO CTRL rats. TNF-α concentrations were significantly higher in the NR OVX groups. 12 weeks of exercise significantly reduced the concentrations of both TNF-α and IL-6 compared to the NR counterparts. The activity of myeloperoxidase enzyme (MPO) was significantly increased as a result of OVX and HT diet, however voluntary wheel-running exercise restored the elevated values. Our results show that estrogen deficiency and HT diet caused a significant decrease in the activity and concentration of HO enzyme, as well as the concentrations of TNF-α, IL-6, and the activity of MPO. However, 12 weeks of voluntary wheel-running exercise is a potential non-pharmacological therapy to ameliorate these disturbances, which determine the life expectancy of postmenopausal women

Multiple Applications of Different Exercise Modalities with Rodents

A large proportion of chronic diseases can be derived from a sedentary lifestyle. Raising physical activity awareness is indispensable, as lack of exercise is the fourth most common cause of death worldwide. Animal models in different research fields serve as important tools in the study of acute or chronic noncommunicable disorders. With the help of animal-based exercise research, exercise-mediated complex antioxidant and inflammatory pathways can be explored, which knowledge can be transferred to human studies. Whereas sustained physical activity has an enormous number of beneficial effects on many organ systems, these animal models are easily applicable in several research areas. This review is aimed at providing an overall picture of scientific research studies using animal models with a focus on different training modalities. Without wishing to be exhaustive, the most commonly used forms of exercise are presented

Sexual Dimorphism of Cardiovascular Ischemia Susceptibility Is Mediated by Heme Oxygenase

We investigated the gender differences in heme-oxygenase (HO) enzyme, which produces endogenous vascular protective carbon monoxide (CO). We studied (1) the activity and expression of HO enzymes in the left ventricle (LV) and aorta, (2) basal increase in basal blood pressure provoked by arginine vasopressine (AVP) in vivo, (3) the heart perfusion induced by AVP, (4) the ST segment depression provoked by adrenaline and 30 seconds later phentolamine, and (5) the aorta ring contraction induced by AVP in female and male Wistar rats. We found that HO activity and the expression of HO-1 and HO-2 were increased in female rat aorta and LV. We demonstrated that the basal blood pressure and administration of AVP provoked blood pressure response are increased in the males; the female myocardium was less sensitive towards angina. Both differences could be aggravated by the inhibition of HO. The aorta rings were more susceptible towards vasoconstriction by AVP in males; isolated heart perfusion decrease was higher in males. The HO inhibition aggravated the heart perfusion in both sexes. In conclusion, the increased HO activity and expression in females might play a role in the sexual dimorphism of cardiovascular ischemia susceptibility during the reproductive age