Carbonic anhydrase (CA) is a metalloenzyme that performs interconversion between CO2 and the bicarbonate ion (HCO3-). CAs appear among all taxonomic groups of three domains of life. Wide spreading of CAs in nature is explained by the fact that carbon, which is the major constituent of the enzyme’s substrates, is a key element of life on the Earth. Despite the diversity of CAs, they all carry out the same reaction of CO2/HCO3- interconversion. Thus, CA obviously represents a universal enzyme of the
carbon-based life. Within the classification of CAs, here we proposed the existence of an extensive family of CA-related proteins (γCA-RPs) - the inactive forms of γ-CAs, which are widespread among the Archaea, Bacteria, and, to a lesser extent, in Eukarya. This review focuses on the history of CAs discovery and integrates the most recent data on their classification, catalytic mechanisms, and physiological roles at various organisms., E. Kupriyanova, N. Pronina, D. Los., and Obsahuje bibliografii
The review incorporates recent information on carbonic anhydrase (CA, EC: 4.2.1.1) pertaining to types, homology, regulation, purification, in vitro stability, and biological functions with special reference to higher plants. CA, a ubiquitous enzyme in prokaryotes and higher organisms represented by four distinct families, is involved in diverse biological processes, including pH regulation, CO2 transfer, ion exchange, respiration, and photosynthetic CO2 fixation. CA from higher plants traces its origin with prokaryotes and exhibits compartmentalization among their organs, tissues, and cellular organelles commensurate with specific functions. In leaves, CA represents 1-20 % of total soluble protein and abundance next only to ribulose-1,5-bisphosphate carboxylase/oxygenase (RuBPCO) in chloroplast, facilitating CO2 supply to phosphoenol pyruvate carboxylase in C4 and CAM plants and RuBPCO in C3 plants. It confers special significance to CA as an efficient biochemical marker for carbon sequestration and environmental amelioration in the current global warming scenario linked with elevated CO2 concentrations. and A. Tiwari ... [et al.].
The leaves of 30-d-old plants of Brassica juncea Czern & Coss cv. Varuna were sprayed with 10-6 M aqueous solutions of indole-3-yl-acetic acid (IAA), gibberellic acid (GA3), kinetin (KIN), and abscisic acid (ABA) or 10-8 M of 28-homobrassinolide (HBR). All the phytohormones, except ABA, improved the vegetative growth and seed yield at harvest, compared with those sprayed with deionised water (control). HBR was most prominent in its effect, generating 32, 30, 36, 70, 25, and 29 % higher values for dry mass, chlorophyll content, carbonic anhydrase (E.C. 4.2.1.1) activity, and net photosynthetic rate in 60-d-old plants, pods per plant, and seed yield at harvest, over the control, respectively. The order of response to various hormones was HBR > GA3 > IAA > KIN > control > ABA. and S. Hayat ... [et al.].
Carcinopodacarus polymorphus gen. n. et sp. n. (Acariformes: Dermationidae: Dermationinae) is described from the guira cuckoo Guira guira (Gmelin) (Cuculiformes: Cuculidae) in Brazil. The new genus differs from the closest genus, Psittophagoides Fain, 1964, by the following features: in both sexes, the anterior spines of trochanters I and II are absent (vs present in Psittophagoides), setae d2 are distinctly developed (vs only alveoli), and genual setae mGI are absent (vs present); in males, the hysteronotal shield is split transversally at the level of trochanters III (vs hysteronotal shield entire); in females, the platelets situated posterior to the propodonotal shield are absent (vs present), the metapodosomal sclerites are present (vs absent), and the adanal shields are fused anteriorly to each other (vs separated from each other). In this species, andropolymorphism is detected for the first time for the family. It involves various characters but the most impressive feature is the structure of legs III. In hetero- and mesomorphic males, these legs are strongly hypertrophied and have a distinct ventral spur on femora III; in homeomorphic males, legs III are not modified and subequal to legs IV., Fabio Akashi Hernandes, Luiz Gustavo A. Pedroso, Andre V. Bochkov., and Obsahuje bibliografii
AT1 receptor (AT1R) blockade prevents physiological cardiac hypertrophy induced by resistance training. Also, our group showed that a single bout of resistance exercise (RE) activates the AKT/mTOR which was also inhibited by AT1R blocker. Here, we investigated whether IGF1-receptor (IGF1-R) and MAPKs were also activated after a single bout of RE. Wistar rats were divided into Sedentary (Sed), Sedentary treated with losartan (Sed+LOS), Exercise (EX), and Exercise treated with losartan (EX+LOS). Cardiac tissue was obtained 5 and 30 min after 4 sets of 12 repetitions of squat exercise (80 % 1RM). We demonstrated that a single bout of RE did not induce IGF1-R tyrosine phosphorylation. ERK1/2 and P38 phosphorylation levels were elevated in the EX 5min and EX 30min groups however, only ERK1/2 was inhibited by losartan treatment (AT1R blocker). Next, we showed that β-arrestin-2 expression increased 28 % in trained animals compared to sedentary group. Altogether, our results demonstrate that AT1R, but not IGF1-R, may exert the hypertrophic cardiac stimulus RE-induced. Also, activation of AKT/mTOR and ERK1/2 pathways may occur through the
β-arrestin-dependent pathway.
Thyroid hormones are powerful modulators of heart function and susceptibility to arrhythmias via both genomic and non-genomic actions. We aimed to explore expression of electrical coupling protein connexin-43 (Cx43) in the heart of rats with altered thyroid status and impact of omega-3 polyunsaturated fatty acids (omega-3) supplementation. Adult male Lewis rats were divided into following six groups: euthyroid controls, hyperthyroid (treated with T3) and hypothyroid (treated with methimazol) with or without six-weeks lasting supplementation with omega-3 (20 mg/100 g/day). Left and right ventricles, septum and atria were used for immunoblotting of Cx43 and protein kinase C (PKC). Total expression of Cx43 and its phosphorylated forms were significantly increased in all heart regions of hypothyroid rats compared to euthyroid controls. In contrast, the total levels of Cx43 and its functional phosphorylated forms were decreased in atria and left ventricle of hyperthyroid rats. In parallel, the expression of PKC epsilon that phosphorylates Cx43, at serine 368, was increased in hypothyroid but decreased in hyperthyroid rat hearts. Omega-3 intake did not significantly affect either Cx43 or PKC epsilon alterations. In conclusion, there is an inverse relationship between expression of cardiac Cx43 and the levels of circulating thyroid hormones. It appears that increased propensity of hyperthyroid while decreased of hypothyroid individuals to malignant arrhythmias may be in part attributed to the changes in myocardial Cx43., B. Szeiffová Bačová, T. Egan Beňová, C. Viczenczová, T. Soukup, H. Rauchová, S. Pavelka, V. Knezl, M. Barančík, N. Tribulová., and Obsahuje bibliografii
The contrasting pattern of cardiac inotropy induced by human peptide endothelin-1 (ET-1) has not been satisfactorily explained. It is not clear whether ET-1 is primarily responsible for increased myocardial ET-1 expression and release with resultant inotropic effects, or for the induction of myocardial hypertrophy and heart failure. There are at least two subtypes of endothelin receptors (ETA and ETB) and the inotropic effects of ET-1 differ depending on the receptor involved. Along with some other groups, we reported significant subtype-ETB endothelin receptor down-regulation in human cardiac cells preincubated with endothelin agonists (Dřímal et al. 1999, 2000). The present study was therefore designed to clarify the subtype-selective mechanisms underlying the inotropic response to ET-1 and to its ETB-selective fragment (8-21)ET-1 in the isolated rat heart. The hearts were subjected to (1-21)ET-1 and to (8-21)ET-1, or to 30 min of stop-flow ischemia followed by 40 min of reperfusion, both before and after selective blockade of endothelin receptors.The present study revealed that both peptides, ET-1 and its (8-21)ET-1 fragment, significantly reduced coronary blood flow in nmolar and higher concentrations. The concomitant negative inotropy and chronotropy were marked after ET-1, while the infusion of the ET-1(8-21) fragment produced a slight but significant positive inotropic effect. Among the four endothelin antagonists tested in continuous infusion only the non-selective PD145065 and ETB1/B2-selective BQ788 (in mmolar concentrations) slightly reduced the early contractile dysfunction of the heart induced by ischemia, whereas ETA-selective PD155080 partially protected the rat heart on reperfusion., J. Dřímal, V. Knezl, J. Dřímal Jr , D. Dřímal, K. Bauerová , V. Kettmann, A.M. Doherty , M. Štefek., and Obsahuje bibliografii
Hypothermic incubation of chicken eggs leads to smaller embryos with enlarged hearts, originally described as hypertrophic. Over the years, however, accumulated evidence suggested that hyperplasia, rather than hypertrophy, is the predominant mechanism of cardiac growth during the prenatal period. We have thus set to reevaluate the hypothermia model to precise the exact cellular mechanism behind cardiac enlargement. Fertilized chicken eggs were incubated at either 37.5 °C (normothermia) or 33.5 °C from embryonic day (ED) 13 onward (hypothermia). Sampling was performed at ED17, at which point wet embryo and heart weight were recorded, and the hearts were submitted to histological examination. In agreement with previous results, the hypothermic embryos were 29% smaller and had hearts 18% larger, translating into a 67% increase in the heart to body weight ratio (P < 0.05 for all parameters). The cell size was essentially the same between control and hypothermic hearts in all regions analysed. Likewise, there was no significant relationship between the cell size and heart weight; however, in the hypothermic hearts, there was a trend showing positive correlation between cell sizes in different cardiac regions and heart weight. Proliferation rate, determined on the basis of anti-phosphohistone H3 immunofluorescence, showed an overall increase in the hypothermic group, reaching statistical significance (P = 0.02, t-test) in the right ventricle. The proliferation rate was similar among different regions of the same heart. However, the correlation between the proliferation rate and heart weight was only small (r2 = 0.007 and r2 = 0.234 for the normothermic and hypothermic group, respectively). We thus
conclude that hyperplasia is the predominant response mechanism in this volume-overload model; mechanistically, decreased heart rate at lower temperature increases the end-diastolic and stroke volume, minimizing the drop in cardiac output through the Frank-Starling mechanism. and Corresponding author: David Sedmera
Cardiac micropotentials are considered to have a predictive value in critical ventricular tachycardia or sudden death. These micropotentials are obtained by numeric filtration of the result of sequential averaging of about 200 systoles (i.e. of measurement at about 3 min interval) which is significantly influenced by known intraindividual ECG variability. It follows from our previous studies that the non-dipolar residue (i.e. the sum of all components of an equivalent source of the heart electrical field with the exception of the first three dominant dipolar components) corresponds by its nature to the cardiac micropotentials, i.e. to late potentials. Verification of this hypothesis utilizing singular value decomposition and replacing the sequential averaging by "surface" averaging of the matrix of synchronously measured ECGs is the aim of this project. The results of the present study can be considered as a confirmation of this hypothesis. These results provide a better understanding of the structure of the body surface potential distribution and for clinical purposes they make it possible to attain cardiac micropotentials (late potentials) from one systole.