In children and adolescents (250 healthy subjects) serum dopamine-beta-hydroxylase (DBH) activity (23.95.2 to 57.117.5 μmol/min/ml) increases with the age between 3-10 years, later it decreases approximately by the age of 10-14 years. At the age of 21 to 60 years DBH level is stable. Our study described decreasing DBH activity in adolescents at the age of 10-14 years in the studied sample of healthy persons. Experimental animals (200 Wistar rats, 5-120 days old) show the same trend of enzymatic activity, similarly as in humans. DBH activity in rats is between 0.850.1 to 2.80.05 μmol/min/ml. This activity is highest in 5-day-old rats; it decreases till the age of 14 days and increases mainly in 14- to 35-day-old animals. Decrease of DBH activity in rats between 35 to 40 days is significant and corresponds to the reduction of DBH activity in adolescent humans (10-14 years). Adult rats (aged 90-120 days) show a stable DBH activity. DBH activity intermediately decreases in 10- to 14-year-old children. This decrease corresponds to the intermediate developmental changes of electrophysiological parameters (decreasing EEG activity in healthy adolescents occurs in 10-14 years old children). Puberty is coupled with intermediate decreasing of DBH activity in man and also in experimental animals in the period of prominent psychological and physiological changes.
The effects of altered thyroid state on the antioxidant defense system in the liver of differently aged rats were examined. Male rats aged 15, 45 and 75 days were treated with L-thyroxine, T4 (40 g/100 g body mass, s.c., one dose per day) for 14 days (finally aged 30, 60 and 90 days, respectively). The following antioxidant defense enzymes were measured: superoxide dismutases (both copper zinc, CuZn-SOD and manganese containing, Mn-SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione-S-transferase (GST), glutathione reductase (GR), as well as the content of low molecular mass antioxidant glutathione (GSH). The effect of T4 on antioxidant defense system in the liver differs with respect to age. T4 treatment decreased CAT and GST activities, as well as the content of GSH in animals aged 60 and 90 days. The same treatment elevated GR activity in rats at 30 days of age, this phenomenon was not observed in older animals. The different response of immature rats to thyroxine compared to older animals could be attributed to the differences in thyroxine metabolism and the developmental pattern. Direct effect of T4 on mature rats can be considered as a part of its overall catabolic action.
The relationships between exercise and metabolites as well as between exercise and sarcoplasmic reticulum function were studied in gastrocnemius muscle of ovariectomized-trained rats. Prolonged moderate-intensity exercise, treadmill up-hill run for 90 min with a 10° incline, decreased the muscle glycogen content. Exercise until exhaustion further lowered the glycogen concentration to 13 % of the control, together with a significant decrease of ATP and glucose-6-phosphate concentrations. Also, Ag+-induced Ca2+release, measured in whole muscle homogenate, showed a 30 % reduction on exhaustion, while Ca2+ uptake was unaffected by this exercise. ATPase activities, of both homogenate and SR vesicles, and Ca2+ transport in the latter preparation were not altered on exhaustion. It could be concluded from these results that muscular fatigue in ovariectomized rats after aerobic exercise is caused by the change in energy supply and Ca2+ release from the SR, this latter possibly due to metabolites generated by the exercise., I. Gigli, L. E. Bussmann., and Obsahuje bibliografii
Unilateral deafferentation induced by transection of the C4-C8 dorsal roots of spinal cord, followed by a complex of abnormal self-mutilating behavior, is interpreted as an animal model of chronic nociception. The objective of our study was to test the differences in tail-flick latency between intact control and unilaterally deafferented animals and to assess the changes in their acute nociceptive sensation. The initial hypothesis was that deafferentation-induced painful sensation might cause stress-induced analgesia that should be manifested as prolonged tail-flick latency. The experiment was carried out on 11 male and 10 female adult Wistar rats. The tail-flick latency was repeatedly measured over a period of 10 consecutive weeks both in the preoperative baseline period and following multiple cervical dorsal rhizotomy. Contrary to our hypothesis, unilateral deafferentation was followed by a significant shortening of the tail-flick latency both in males and females. In deafferented animals, compared to the controls, variations of tail-flick latency were reduced. In individual animals after deafferentation, concurrent dynamic changes were observed in self-mutilating behavior, in a loss and regaining of body weight, and in tail-flick latency. Our data suggest that changes in tail-flick latency may be interpreted in terms of central sensitization and that tail-flick latency might be considered as a useful marker of chronic nociception.
Autophagy is implicated in the maintenance of cardiac homeostasis. Autophagy is activated in heart failure, in which reactive oxygen species (ROS) are increased. Exogenous ROS have been shown to induce cardiomyocyte autophagy alterations. However, little is known about the influences of physiological levels of endogenous ROS on cardiomyocyte autophagy. In the present study, we tested the hypothesis that endogenous ROS in cardiomyocytes play an important role in inducing autophagy. Cultured H9C2 cardiomyocytes or Sprague-Dawley rats were treated with the antioxidant N-acetyl-cysteine (NAC) or the superoxide dismutase mimic tempol under the basal or nutrient deprivation conditions. The autophagic flux was assessed by the lysosomal inhibitor chloroquine. In H9C2 cardiomyocytes, under a basal condition, NAC or tempol increased the ratio of LC3 II/I proteins and reduced LC3 II autophagic flux. Under nutrient deprivation, NAC increased the LC3 II/I ratio and reduced LC3 II autophagic flux. In vivo studies in rats, NAC treatment increased the LC3 II/I ratio and p-Akt protein expression in myocardium. We concluded that the antioxidants reduced autophagic flux in cardiomyocytes under the basal or nutrient deprivation conditions, suggesting that endogenous ROS promote autophagy flux under physiological conditions, and this effect is mediated, at least in part, through Akt inhibition., J.-P. Wang, R.-F. Chi, J. Liu, Y.-Z. Deng, X.-B. Han, F.-Z. Qin, B. Li., and Seznam literatury