Two weeks-old maize (Zea mays cv. XL-72.3) plants were exposed to Al concentrations 0 (Al0), 9 (Al9), 27 (Al27) or 81 (Al81) g m-3 for 20 d in a growth medium with low ionic strength. Thereafter, the Al concentration-dependent interactions on root nitrate uptake, and its subsequent reduction to ammonia in the leaves were investigated. Al concentrations in the roots sharply increased with increasing Al concentrations while root elongation correspondingly decreased. Root fresh and dry masses, acidification capacity, and nitrate and nitrogen contents decreased from Al27 onwards, whereas leaf nitrogen, nitrate, nitrite, and ammonia concentrations decreased starting with Al9. Electrolytic conductance increased by 60 % in root tissues from Al0 to Al81 but it did not increase significantly in the leaves. In Al9, Al27, and Al81 plants a decrease in shoot fresh and dry masses was observed. Al concentrations between 0 and 27 g m-3 increased net photosynthetic rate, stomatal conductance, and the quantum yield of photosynthetic electron transport, whereas the intercellular CO2 concentration was minimum in Al27 plants. In the leaves, nitrate reductase (E.C. 1.6.6.1) activity increased until Al27, and nitrite reductase (E.C. 1.6.6.4) activity until Al81. Hence there may be an Al mediated extracellular and intracellular regulation of root net nitrate uptake. Nitrate accumulation in the roots affects the translocation rates and, therefore, the nitrate concentration in the leaves. The in vivo reducing power generated by the photosynthetic electron flow does not limit nitrate to ammonia reduction, and the increase of maximum nitrate and nitrite reductase activities parallels the decreasing nitrate, nitrite, and ammonia concentrations. and F. C. Lidon, J. C. Ramalho, M. G. Barreiro.
In laboratory experiments, conspecific excretions and ammonia solutions evoked avoidance reactions in tadpoles of three anuran species, Bufo bufo, Rana temporaria, and Rana arvalis . A differential sensitivity of ammonia chemoreception was determined for two anuran species. For Bufo bufo tadpoles, these characteristics at ammonia backgr ound concentration of 0.2 mg/l lied in the range 150 % < dI/I < 500 %, and for background of 0.4 mg/l the value lied in th e range 400 % < dI/I < 500 %. For Rana temporaria tadpoles, differential threshold against ammonia background concentration of 0. 15 mg/l was close to 200 % and against background ammonia concentration of 1.1 mg/l was close to 100 %. These results suggest that such sensitivity of both anurans is sufficient for using ammonia in intra- and interspecies communication., Y. B. Manteifel, E. I. Kiseleva., and Obsahuje bibliografii a bibliografické odkazy
Histidine (HIS) is investigated for therapy of various disorders and as a nutritional supplement to enhance muscle performance. We examined effects of HIS on amino acid and protein metabolism. Rats consumed HIS in a drinking water at a dose of 0.5 g/l (low HIS), 2 g/l (high HIS) or 0 g/l (control) for 4 weeks. At the end of the study, the animals were euthanized and blood plasma, liver, soleus (SOL), tibialis (TIB), and extensor digitorum longus (EDL) muscles analysed. HIS supplementation increased food intake, body weight and mass and protein contents of the liver and kidneys, but not muscles. In blood plasma there were increases in glucose, urea, and several amino acids, particularly alanine, proline, aspartate, and glutamate and in high HIS group, ammonia was increased. The main findings in the liver were decreased concentrations of methionine, aspartate, and glycine and increased alanine. In muscles of HIS-consuming animals increased alanine and glutamine. In high HIS group (in SOL and TIB) increased chymotrypsin-like activity of proteasome (indicates increased proteolysis); in SOL decreased anserine (beta-alanyl-N1-methylhistidine). We conclude that HIS supplementation increases ammonia production, alanine and glutamine synthesis in muscles, affects turnover of proteins and HIScontaining peptides, and increases requirements for glycine and methionine.
Histidine (HIS) is an essential amino acid investigated for therapy of various diseases, used for tissue protection in transplantation and cardiac surgery, and as a supplement to increase muscle performance. The data presented in the review show that HIS administration may increase ammonia and affect the level of several amino acids. The most common are increased levels of alanine, glutamine, and glutamate and decreased levels of glycine and branched-chain amino acids (BCAA, valine, leucine, and isoleucine). The suggested pathogenic mechanisms include increased flux of HIS through HIS degradation pathway (increases in ammonia and glutamate), increased ammonia detoxification to glutamine and exchange of the BCAA with glutamine via L-transporter system in muscles (increase in glutamine and decrease in BCAA), and tetrahydrofolate depletion (decrease in glycine). Increased alanine concentration is explained by enhanced synthesis in extrahepatic tissues and impaired transamination in the liver. Increased ammonia and glutamine and decreased BCAA levels in HIS-treated subjects indicate that HIS supplementation is inappropriate in patients with liver injury. The studies investigating the possibilities to elevate carnosine (β-alanyl-L-histidine) content in muscles show positive effects of β-alanine and inconsistent effects of HIS supplementation. Several studies demonstrate HIS depletion due to enhanced availability of methionine, glutamine, or β-alanine., Milan Holeček., and Obsahuje bibliografii
Uric acid is involved in nitrogenous waste in animals, together with ammonia and urea. Uric acid has also antioxidant properties and is a surrogate marker of metabolic syndrome. We observed that the elevated plasma uric acid of high-fat fed mice was normalized by benzylamine treatment. Indeed, benzylamine is the reference substrate of semicarbazide-sensitive amine oxidase (SSAO), an enzyme highly expressed in fat depots and vessels, which generates ammonia when catalysing oxidative deamination. Ammonia interferes with uric acid metabolism/solubility. Our aim was therefore to investigate whether the lowering action of benzylamine on uric acid was related to an improvement of diabetic complications, or was connected with SSAO-dependent ammonia production. First, we observed that benzylamine administration lowered plasma uric acid in diabetic db/db mice while it did not modify uric acid levels in normoglycemic and lean mice. In parallel, benzylamine improved the glycemic control in diabetic but not in normoglycemic mice, while plasma urea remained unaltered. Then, uric acid plasma levels were measured in mice invalidated for AOC3 gene, encoding for SSAO. These mice were unable to oxidize benzylamine but were not diabetic and exhibited unaltered plasma uric levels. Therefore, activated or abolished ammonia production by SSAO was without influence on uric acid in the context of normoglycemia. Our observations confirm that plasma uric acid increases with diabetes and can be normalized when glucose tolerance is improved. They also show that uric acid, a multifunctional metabolite at the crossroads of nitrogen waste and of antioxidant defences, can be influenced by SSAO, in a manner apparently related to changes in glucose homeostasis., C. Carpéné ... [et al.]., and Obsahuje seznam literatury