We assessed the effects of nutrient enrichment on three stream ecosystems running through distinct biomes (Mediterranean, Pampean and Andean). We increased the concentrations of N and P in the stream water 1.6-4-fold following a before-after control-impact paired series (BACIPS) design in each stream, and evaluated changes in the biomass of bacteria, primary producers, invertebrates and fish in the enriched (E) versus control (C) reaches after nutrient addition through a predictive-BACIPS approach. The treatment produced variable biomass responses (2-77% of explained variance) among biological communities and streams. The greatest biomass response was observed for algae in the Andean stream (77% of the variance), although fish also showed important biomass responses (about 9-48%). The strongest biomass response to enrichment (77% in all biological compartments) was found in the Andean stream. The magnitude and seasonality of biomass responses to enrichment were highly site specific, often depending on the basal nutrient concentration and on windows of ecological opportunity (periods when environmental constraints other than nutrients do not limit biomass growth). The Pampean stream, with high basal nutrient concentrations, showed a weak response to enrichment (except for invertebrates), whereas the greater responses of Andean stream communities were presumably favored by wider windows of ecological opportunity in comparison to those from the Mediterranean stream. Despite variation among sites, enrichment globally stimulated the algal-based food webs (algae and invertebrate grazers) but not the detritus-based food webs (bacteria and invertebrate shredders).Environ. Res. Lett. 8 (2013) 014002 J Artigas et al nutrient enrichment tends to globally enhance the biomass of stream biological assemblages, but that its magnitude and extent within the food web are complex and are strongly determined by environmental factors and ecosystem structure.
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Oxytocin (OT) prohormone processing was studied in fetal sheep. Using specific antisera that recognize the amidated and the COOH-terminal extended forms of OT, we measured arterial and venous levels of the OT peptides in fetal sheep plasma at 94 and 138 days of gestation. Plasma levels of the COOH-terminal extended forms, OT-X, were highest early in development, 35.7 +/- 9.8 vs. 14.3 +/- 5.7 pg/ml (94 vs. 138 days). The ratio of the plasma peptides, OT-X to OT, was higher in the young fetus (35 +/- 11.6 vs. 3.1 +/- 1.3, 94 vs. 138 days). There were also developmental changes in the umbilical artery-umbilical vein differences, with positive values noted in late gestation. These results demonstrate that the changes in the processing of the OT precursor that occur during fetal development are reflected by alterations in the relative amounts of prohormone and amidated hormone found in fetal plasma.
Ketamine-HCl has been reported, depending on experimental conditions and dosage given, to have significant cardiovascular and endocrine effects in some species. However, previous studies in primates have inadequately distinguished between animal handling and ketamine effects. We, therefore, examined the effects of various doses of ketamine (0, 5 , 10, 15, and 20 mg/kg) on mean arterial blood pressure and on plasma insulin, glucose, and cortisol concentrations in 10 chronically cannulated Macaca fascicularis monkeys which had been acclimated to restraining chairs. Each monkey received three different doses of ketamine according to a balanced incomplete block design. Ketamine anesthesia produced no significant changes in plasma insulin, glucose, or cortisol concentrations nor did it affect mean arterial blood pressure. In addition, the effects of ketamine-HC1 on endocrine responses to insulin-induced hypoglycemia were examined in four animals according to a cross-over design. These animals also had chronically maintained cannulas and had been acclimated to restraining chairs. Plasma glucose concentrations, as well as plasma ACTH, growth hormone, and cortisol responses in ketamine-anesthetized animals receiving an insulin challenge were no different from those in unanesthetized control animals. Thus, our studies indicate that ketamine-HCl does not perturb these particular hormonal systems in M. fuscicularis monkeys. 389
Information on total and free serum thyroid hormone concentrations in the adult and fetal guinea pig (Cavia porcellus) is limited. These variables were studied in adult male and female guinea pigs and in pregnant guinea pigs and their fetuses at various times during gestation. Total serum T4 levels in adult males, nonpregnant females, and pregnant females did not differ significantly [range, 2.5 +/- 0.3 to 3.2 +/- 0.8 micrograms/dl (mean +/- SD)]. Similarly, there were no significant differences in the percent free T4 (0.046-0.068%), free T4 (1.26-2.03 ng/dl), total T3 (39-44 ng/dl), the percent free T3 (0.521-0.638%), and free T3 (0.221-0.260 ng/dl) among adult males, nonpregnant females, and pregnant females. rT3 was undetectable in adult male, nonpregnant female, and pregnant female guinea pig serum. T4 values were similar and those for T3 were lower in fetal compared to maternal serum at 45 days of gestation, whereas serum rT3 was detectable in fetal serum. Between 45 and 62 days of gestation, fetal serum T4 increased from 2.5 to 0.3 to 4.3 +/- 1.3 micrograms/dl (mean +/- SD, P less than 0.01), fetal serum T3 remained unchanged, and fetal serum rT3 increased from 5.2 +/- 3.3 to 25.0 +/- 11.4 ng/dl (P less than 0.01). Near term, fetal serum total and free T4 and total rT3 concentrations were significantly higher and total and free T3 concentrations were significantly lower than the corresponding values in maternal serum. Total serum T4 is higher in the guinea pig than in the rabbit, is similar to values in the rat, and is lower than values in man. The free T4 concentration in guinea pig serum is similar to those in humans and rats. The ontogenesis of thyroid hormones differs strikingly in the guinea pig fetus compared to that in the rat fetus and shares many similarities with sheep and human fetal thyroid development.
The placenta contains iodothyronine 5-deiodinase activity (P5-Dase) that probably acts on iodothyronines in the fetal circulation to convert T4 to rT3 and T3 to 3,3'-T2. Since thyroid status and fasting have profound effects on iodothyronine deiodinases in other tissues, the present studies were performed to determine if these perturbations affected P5-Dase. Control and treated rats were mated and killed near term on the 20th day of gestation. P5-Dase was determined in placenta homogenates enriched with dithiothreitol by measuring the conversion of T4 to rT3. In four of five studies, P5-Dase was similar in dams that underwent thyroidectomy (Tx) on day 7 of gestation and sham Tx dams. P5-Dase was not altered in dams that were treated with methimazole (MMI) to induce maternal and fetal hypothyroidism. Treatment of dams with supraphysiological doses of T4, beginning on the seventh day of gestation, did not significantly affect P5-Dase. In three of four studies, P5-Dase was similar in fed dams to values in dams fasted for the last 5 days of pregnancy. Placenta iodothyronine 5'-deiodinase activity (P5'-Dase) was also measured in some studies. P5'-Dase was not decreased in Tx rats and was modestly decreased in MMI-treated rats. However, the effect of MMI was not reversed by the administration of supraphysiological doses of T4, Tx, MMI treatment, and fasting all decreased hepatic T4 5'-deiodinase activity in pregnant rats. These results strongly suggest that thyroid status and fasting do not alter P5-Dase activity.
IntroductionBroken cell preparations of rat and human placentas contain an inner (tyrosyl)-ring iodothyronine deiodinase enzyme with greatest activity when the substrate is 3,5,3'-triiodothyronine (T3). This report describes the deiodination of T3 in the intact placenta and the effect of sodium iopanoate (IA) and propylthiouracil (PTU) on T3 deiodination. Under nembutal anesthesia, the placenta of60-65-d-old pregnant guinea pigs was surgically exposed, a single umbilical artery and the umbilical vein were cannulated, and the fetus was removed. In a temperature-controlled chamber (37°C), the fetal side of the placenta was perfused through the umbilical artery at a rate of 1 ml/min with 3% bovine serum albumin Krebs-Henseleit buffer containing 0.14 nM outer ring labeled 1'"IJT3. Placenta effluent fractions were collected at timed intervals from the umbilical vein canulla throughout a 120-min perfusion period. The contents of the perfusion buffer and the various effluent fractions were analyzed for their iodothyronine content by high pressure liquid chromatography. In five experiments, the percent composition of '25I-labeled iodothyronines in the perfusion buffer and placenta effluent was 95.3±1.0 (mean±SE) and 70.2±2.1 for T3 (P < 0.01), 2.5±0.7 and 20.1±1.8 for 3,3'-T2 (P < 0.01), and 0 and 8.2±0.9 for 3'-Ti. The placenta receives a large percentage of the fetal cardiac output (1), and, as we and others have reported (2-7), contains enzymes that deiodinate thyroid hormones. These observations support the possibility that the placenta is an important site for fetal thyroid hormone metabolism. Deiodination of the iodothyronines can occur in the phenolic (5' or outer) or in the tyrosyl (5 or inner) rings. These deiodinative pathways play a major role in the metabolism of thyroxine (T4),' generating the metabolically active iodothyronine, 3,5,3'-triiodothyronine (T3), and the metabolically inactive iodothyronine, 3,3',5'-triiodothyronine (rT3). Deiodination is also the principal pathway for the metabolism of T3, which results in the formation of the inactive diiodothyronines, 3,3'-T2 and 3,5-T2, as well as the inactive monoiodothyronines, 3'-T, and 3-T1. Thus, placental deiodination is potentially an important mechanism for the modulation of fetal thyroid hormone action. While detailed studies of deiodination have been performed in placenta homogenates and subcellular fractions (6,8), there is little information on iodothyronine deiodination in the intact placenta (9).In this study, we discovered the metabolic fate of T3 when perfused through the fetal side ofthe guinea pig placenta in situ. Since previous studies employing placenta homogenates have shown an inhibitory effect ofpropylthiouracil (PTU) and sodium iopanoate (IA) on T4 deiodination (8), the effect of these drugs on T3 metabolism in the intact placenta was evaluated.
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