Carbon disulfide exposure attenuates adrenergic inotropic response in rats

Catecholamine-induced myocardial necrosis is enhanced in carbon disulfide exposed rats. We investigated whether the reported morphological findings after carbon disulfide exposure are accompanied by functional disturbances of the adrenergic inotropic response as well as by biochemical alterations. The cardiac effects of epinephrine and norepinephrine were studied in urethane-anesthetized rats which had been subacutely exposed to carbon disulfide. Compared with not exposed control animals left ventricular inotropic response was diminished and the transient T-wave elevation of the ECG due to ischemic episodes was enhanced in carbon disulfide-exposed rats. Activity of LDH-isozymes in the myocardium was shifted toward LDH-M. Our results support the hypothesis that carbon disulfide causes disturbances of energy supply in the heart.     

Antioxidative and metabolic responses to extended cold exposure in rats

In this work, we investigated whether extended cold exposure increases oxidative damage and susceptibility to oxidants of rat liver, heart, kidney and lung which are metabolically active tissues. Moreover in this study the effect of cold stress on some of the lipid metabolic mediators were studied in rat experimental model. Male albino Sprague-Dawley rats were randomly divided into two groups: The control group (n=12) and the cold-stress group (n=12). Tissue superoxide dismutase (SOD), catalase (CAT), glutathion S-transferase (GST) and glutathion reductase (GR) activities and glutathion (GSH) were measured using standard protocols. The biochemical analyses for total lipid, cholesterol, trigliceride, HDL, VLDL and LDL were done on autoanalyzer. In cold-stress groups SOD activity was decreased in the lung whereas it increased in the heart and kidney. CAT activity was significantly decreased (except liver) in all the tissues in treated rats. GST activity of cold-induced rats increased in liver and heart while decreased in the lung. GR activity was significantly decreased (except in liver) in all the tissues in cold-stressed rats. GSH level was significantly increased in the heart but decreased in the lung of animals exposed to cold when compared to controls. It was found that among the groups trigliceride, total lipid, HDL and VLDL parameters varied significantly but cholesterol and LDL had no significant variance. In this study, we found that exposure of extended (48 h) cold (8 degrees C) caused changes both in the antioxidant defense system (as tissue and enzyme specific) and serum lipoprotein profiles in rats.     

Odour-mediated responses of phytophagous mites to conspecific and heterospecific competitors

Plants under herbivore attack produce volatiles, thus attracting natural enemies of the herbivores. However, in doing so, the plant becomes more conspicuous to other herbivores. Herbivores may use the odours as a cue to refrain from visiting plants that are already infested, thereby avoiding competition for food, or, alternatively, to visit plants with defences weakened by earlier attacks. We investigated the response of one species of herbivore (the spider mite Tetranychus urticae) to odours emanating from cucumber plants infested by conspecific or heterospecific (the western flower thrips, Frankliniella occidentalis) herbivores. Olfactometer experiments in the laboratory showed that spider mites have a slight, but significant, preference for plants infested with conspecifics, but strongly avoid plants with thrips. These results were substantiated with greenhouse experiments. We released spider mites on the soil in the centre of a circle of six plants, half of which were infested with either conspecifics or heterospecifics (thrips), whereas the other half were uninfested. It was found that 60–70% of the mites were recaptured on the plants within 5 h after release. Results of these experiments were in agreement with results of the olfactometer experiments: (1) significantly fewer spider mites were found on plants infested with thrips than on uninfested plants and (2) more mites were found on plants with conspecifics than on clean plants (although this difference was not significant). From a functional point of view it makes sense that spider mites prefer clean plants over thrips-infested plants, since thrips are not only competitors, but are also known as intraguild predators of spider mites. Possible reasons for the slight attraction of spider mites to plants infested with conspecifics are discussed. Received: 22 June 1996 / Accepted: 29 September 1996     

Sex-and age-dependent effects of prenatal exposure to caffeine on open-field behavior, emergence latency and adrenal weights in rats

Pregnant rats were provided with drinking water containing 0, 0.23 or 0.3 mg/ml of caffeine throughout gestation. These concentrations gave rise to daily doses of 0, 28 and 36 mg/kg. Open-field behavior and latencies to emerge from a darkened chamber were observed in offspring at regular intervals from 1 to 8 months after birth. The main results revealed increases in open-field locomotor and rearing activity with 28 but not 36 mg/kg/day. The opposite pattern characterized emergence latency. These changes were more typical of male rats particularly when older. Combining the present results with those of an earlier study by the authors strengthened the curvilinear trends observed and led to the conclusion that, low doses of prenatal caffeine increase activity and decrease emotionality. Higher doses may have the opposite effects to the point that the significant differences from control subjects reported earlier can occur. When 8 months old, female but not male rats prenatally exposed to 36 mg/kg/day of caffeine had significantly heavier adrenal glands than controls.     

Embryonic exposure to conspecific chemicals suppresses cane toad growth and survival

Adaptations to suppress the viability of conspecifics may provide novel ways to control invasive taxa. The spread of cane toads (Rhinella marina) through tropical Australia has had severe ecological impacts, stimulating a search for biocontrol. Our experiments show that cane toad tadpoles produce waterborne chemical cues that suppress the viability of conspecifics encountering those cues during embryonic development. Brief (72 h) exposure to these cues in the egg and post-hatching phases massively reduced rates of survival and growth of larvae. Body sizes at metamorphosis (about three weeks later) were almost twice as great in control larvae as in tadpole-exposed larvae. The waterborne cue responsible for these effects might provide a weapon to reduce toad recruitment within the species' invaded range.     

Escape and aggregation responses of three echinoderms to conspecific stimuli.

In marine invertebrates, waterborne chemical stimuli mediate responses including prey detection and predator avoidance. Alarm and flight, in response to damaged conspecifics, have been reported in echinoderms, but the nature of the stimuli involved is not known. The responses of Asterias rubens Linnaeus, Psammechinus miliaris (Gmelin), and Echinus esculentus Linnaeus to conspecifics were tested in a choice chamber against a control of clean seawater (no stimulus). All three species showed statistically significant movement toward water conditioned by whole animals or homogenate of test epithelium. P. miliaris and E. esculentus displayed a statistically significant avoidance reaction, moving away from conspecific coelomic fluid, gut homogenate, and gonad homogenate. A. rubens was indifferent to conspecific coelomic fluid, pyloric cecum homogenate, and gonad homogenate but moved away from cardiac gut homogenate. P. miliaris was indifferent to gametes, but the other two species were significantly attracted to them. No species showed preference for one particular side of the chamber during trials to balance water flow. These echinoderms can distinguish between homogenates of conspecific tissues that might be exposed when a predator damages the test, and those that may emanate from the exterior surface during normal activities.     

Cyclosporine attenuates the autonomic modulation of reflex chronotropic responses in conscious rats

Cyclosporine A (CyA), an immunosuppressant drug, has been shown to attenuate the baroreflex control of heart rate (HR). This study investigated whether or not the CyA-induced baroreflex dysfunction is due to alterations in the autonomic (sympathetic and parasympathetic) control of the heart. We evaluated the effect of muscarinic or beta-adrenergic blockade by atropine and propranolol, respectively, on reflex HR responses in conscious rats treated with CyA (20 mg x kg(-1) x day(-1) dissolved in sesame oil) for 11-13 days or the vehicle. Baroreflex curves relating changes in HR to increases or decreases in blood pressure (BP) evoked by phenylephrine (PE) and sodium nitroprusside (NP), respectively, were constructed and the slopes of the curves were taken as a measure of baroreflex sensitivity (BRS(PE) and BRS(NP)). Intravenous administration of PE and NP produced dose-related increases and decreases in BP, respectively, that were associated with reciprocal changes in HR. CyA caused significant (P < 0.05) reductions in reflex HR responses as indicated by the smaller BRS(PE) (-0.97 +/- 0.07 versus -1.47 +/- 0.10 beats x min(-1) x mmHg(-1) (1 mmHg = 133.322 Pa)) and BRS(NP) (-2.49 +/- 0.29 versus -5.23 +/- 0.42 beats x min(-1) x mmHg(-1)) in CyA-treated versus control rats. Vagal withdrawal evoked by muscarinic blockade elicited significantly lesser attenuation of BRS(PE) in CyA compared with control rats (40.2 +/- 8.0 versus 57.7 +/- 4.4%) and abolished the BRS(PE) difference between the two groups, suggesting that CyA reduces vagal activity. CyA also appears to impair cardiac sympathetic control because blockade of beta-adrenergic receptors by propranolol was less effective in reducing reflex tachycardic responses in CyA compared with control rats (41.6 +/- 4.2 versus 59.5 +/- 4.5%). These findings confirm earlier reports that CyA attenuates the baroreceptor control of HR. More importantly, the study provides the first pharmacological evidence that CyA attenuates reflex chronotropic responses via impairment of the autonomic modulation of the baroreceptor neural pathways.     

Experiential and endocrine dependence of gonadotropin responses in male mice to conspecific urine

Previous research has shown that a urinary pheromone of female mice acts via the vomeronasal organ of the accessory olfactory system to elicit rapid release of luteinizing hormone (LH) in conspecific males. Several experiments were conducted to examine the importance of sexual experience for gonadotropin responses in male mice to female urine, male urine, saline, or mixtures of these stimuli. Both sexually naive and sexually experienced male mice had significantly higher plasma LH levels after presentations of female urine than after presentations of male urine. However, sexual experience appeared to increase the reliability of the short-latency gonadotropin response to female urine relative to a sexually neutral component of urine such as sodium chloride, and male urine appeared to suppress spontaneous LH secretion episodes in both naive and sexually experienced males. Subsequent experiments with sexually experienced subjects demonstrated that male mouse urine is a powerful suppressant of LH release in other males. Specifically, female mouse urine mixed with male urine failed to elicit LH responses in male subjects, whereas female urine mixed with saline was highly effective. Urine obtained from castrated male donors was as potent as urine from intact males in suppressing the gonadotropin response to female urine. The suppressive activity in male mouse urine thus does not appear to be critically dependent on gonadal hormones. The existence of a potent stimulatory pheromone in female urine and a potent suppressive pheromone in male urine makes male mice an excellent model system for studying the neural regulation of LH secretion.     

Continuous interferon-gamma or tumor necrosis factor-alpha exposure of enterocytes attenuates cell death responses

Short-term stimulation (i.e. <2 days) with tumor necrosis factor-alpha (TNF-alpha) or interferon-gamma (IFN-gamma) cause growth arrest and sensitize epithelial cells to CD95 (Fas/Apo-1)-mediated cell death. The effect of long-term cytokine exposure on viability, proliferation, and apoptosis response of colonic epithelial cells is unknown and addressed in this study. In the present study HT29 and DLD-1 colonic cells were stimulated with either TNF-alpha or IFN-gamma at varying concentrations for 2-9 days. Viability and proliferation was assessed. CD95-mediated cell death response was determined. IFN-gamma caused decreased viability at high concentrations (1 nM), whereas lower concentrations (10-100 pM) only caused a transient growth arrest. TNF-alpha (100 pM) did not affect cell growth. Cells stimulated for 8 days with IFN-gamma (10 pM) or TNF-alpha (100 pM) had higher proliferation rates than controls or cells stimulated for 2 days (p < 0.05). Whereas the spontaneous cell death increased slightly during continuous cytokine exposure the CD95L response decreased (P < 0.01). Colonic cells continuously exposed to IFN-gamma or TNF-alpha had cell turnover characteristics that resemble findings in patients with UC. Increased proliferation and decreased cell death response may act as a counter regulatory mechanism that limits the damaging effects of cytokines.     

Terguride attenuates prolactin levels and ameliorates insulin sensitivity and insulin binding in obese spontaneously hypertensive rats

Glucose tolerance, serum insulin, insulin receptors in epididymal fat tissue, circulating total cholesterol and triglyceride concentrations as well as serum prolactin were studied in obese and lean spontaneously hypertensive rats (SHR) of both sexes. Obese animals displayed insulin resistance and elevated insulin and triglyceride concentrations. Moreover, in obese rats the increased mass of epididymal fat tissue was accompanied with decreased capacity of high affinity binding sites of insulin receptors in the tissue plasma membranes. Terguride treatment lowered prolactin serum levels which was accompanied by ameliorated insulin sensitivity in obese animals of both sexes. In addition, terguride treatment decreased serum insulin and triglyceride concentrations in obese females and at the same time enhanced the affinity of high affinity insulin binding sites. Our results show that obesity in SHR is associated with a decreased capacity of insulin receptors and that prolactin may play a role in obesity-induced insulin resistance, particularly in female rats.     

Lifelong exposure to dietary fish oil alters macrophage responses in Walker 256 tumor-bearing rats

Supplementation of the diet with fish oil (FO) decreases growth of the Walker 256 tumor and decreases the cachexia associated with tumor-bearing. The mechanisms by which FO inhibits tumor growth and cachexia are unknown. Macrophages are very important in host defence against tumors since they produce several anti-tumor agents which in turn have been shown to be modified by dietary FO, but rarely in the setting of tumor bearing and never in relation to lifelong exposure. In this study, we compared the effects of supplementation of the diet of pregnant and lactating rats and subsequent supplementation of the offspring with coconut fat or FO on macrophage activities involved in anti-tumor defence. FO supplementation was able to induce an increase in phagocytosis, in O2-, H2O2, nitric oxide, and TNF-alpha production by macrophages and in lysosomal volume in non-tumor-bearing rats. However, phagocytosis, production of O2- and H2O2 and lysosomal volume were not affected by the FO diet when rats were bearing tumors, although nitric oxide production was higher in these animals. It appears that tumor bearing activates the innate immune system and that dietary FO has little effect on innate immunity in the presence of Walker 256 tumors. Thus, it is still unclear how FO decreases the growth of Walker 256 tumors and the associated cachexia.     

Prenatal exposure to bisphenol A promotes angiogenesis and alters steroid-mediated responses in the mammary glands of cycling rats

Prenatal exposure to BPA disturbs mammary gland histoarchitecture and increases the carcinogenic susceptibility to chemical challenges administered long after BPA exposure. Our aim was to assess the effect of prenatal BPA exposure on mammary gland angiogenesis and steroid hormone pathways in virgin cycling rats. Pregnant Wistar rats were exposed to either 25 or 250 g/kg/day (25 and 250 BPA, respectively) or to vehicle. Female offspring were autopsied on postnatal day (PND) 50 or 110. Ovarian steroid serum levels, the expression of steroid receptors and their co-regulators SRC-3 and SMRT in the mammary gland, and angiogenesis were evaluated. At PND 50, all BPA-treated animals had lower serum levels of progesterone, while estradiol levels remained unchanged. The higher dose of BPA increased mammary ERα and decreased SRC-3 expression at PND 50 and PND 110. SMRT protein levels were similar among groups at PND 50, whereas at PND 110, animals exposed to 250 BPA showed a lower SMRT expression. Interestingly, in the control and 25 BPA groups, SMRT increased from PND 50 to PND 110. At PND 50, an increased vascular area associated with higher VEGF expression was observed in the 250 BPA-treated rats. At PND 110, the vascular area was still increased, but VEGF expression was similar to that of control rats. The present results demonstrate that prenatal exposure to BPA alters the endocrine environment of the mammary gland and its angiogenic process. Increased angiogenesis and altered steroid hormone signals could explain the higher frequency of pre-neoplastic lesions found later in life. This article is part of a Special Issue entitled 'Endocrine disruptors'.     

Central angiotensin receptor blockade impairs thermolytic and dipsogenic responses to heat exposure in rats

The effect of central angiotensin AT(1) receptor blockade on thermoregulation and water intake after heat exposure was investigated. Rats were placed in a chamber heated to 39 +/- 1 degrees C for 60 min and then returned to their normal cage (at 22 degrees C), and water intake was measured for 120 min. Artificial cerebrospinal fluid (5 microl) was injected intracerebroventricularly 60 min before heat exposure in five control rats. Colonic temperature increased from 37.22 +/- 0.21 to 40.68 +/- 0.31 degrees C after 60 min. In six rats injected intracerebroventricularly with 10 microg of the AT(1) antagonist losartan, colonic temperature increased from 37.41 +/- 0.27 to 41.72 +/- 0.28 degrees C after 60 min. This increase was significantly greater than controls (P < 0.03). Losartan-treated rats drank 1.1 +/- 0.4 ml of water compared with 5.9 +/- 0.77 ml (P < 0.002) drank by control animals, despite a similar body weight loss in the two groups. Central losartan did not inhibit the drinking response to intracerebroventricular carbachol in heated rats, suggesting that losartan treatment did not nonspecifically depress behavior. We conclude that central angiotensinergic mechanisms have a role in both thermoregulatory cooling in response to heat exposure and also the ensuing water intake.     

Cholecystokinin tetrapeptide,proglumide and open-field behavior in rats

The effect of cholecystokinin tetrapeptide (CCK-4) was studied in an open field situation. CCK-4 increased locomotion and rearing and the effect was enhanced by proglumide, a selective antagonist of CCK-8. This is in sharp contrast to our earlier findings that CCK-8 decreased the open-field behavior and that proglumide completely blocked the effect. Thus, the effects of CCK-4 and CCK-8 appear to be opposite to each other in that one is excitatory and the other inhibitory to open-field responses.     

Calcemic responses of Varanus flavescens to prolactin administration

The daily intraperitoneal injections of ovine prolactin to Varanus flavescens (10 I.U./0.2 ml/100 g body wt for 7 days) induced a rise in serum calcium which persisted until the end of the experiment.     

A game theoretical approach to conspecific brood parasitism

We constructed a game theoretical model to predict optimal patternsof egg laying in systems where individuals lay in the nestsof others as well as in their own nests. We show that decreasingthe effect of position within an egg-laying sequence on theworth of an egg should lead to reduced parasitism. Indeed,parasitism can only flourish if the worth of an egg to its biological parent declines with the total number of eggs laid in that nest.Further, we found that increasing the intrinsic costs of eggproduction should lead to an increased propensity for conspecificbrood parasitism. The model also predicts that variation inhosts' ability to reject parasitic eggs has little effect on parasitism until this ability is well developed.     

Cyclooxygenase inhibition attenuates sympathetic responses to muscle stretch in humans

Passive muscle stretch performed during a period of post-exercise muscle ischemia (PEMI) increases muscle sympathetic nerve activity (MSNA), and this suggests that the muscle metabolites may sensitize mechanoreceptors in healthy humans. However, the responsible substance(s) has not been studied thoroughly in humans. Human and animal studies suggest that cyclooxygenase products sensitize muscle mechanoreceptors. Thus we hypothesized that local cyclooxygenase inhibition in exercising muscles could attenuate MSNA responses to passive muscle stretch during PEMI. Blood pressure (Finapres), heart rate, and MSNA (microneurography) responses to passive muscle stretch were assessed in 13 young healthy subjects during PEMI before and after cyclooxygenase inhibition, which was accomplished by a local infusion of 6 mg ketorolac tromethamine in saline via Bier block. In the second experiment, the same amount of saline was infused via the Bier block. Ketorolac Bier block decreased prostaglandin synthesis to approximately 34% of the baseline. Before ketorolac Bier block, passive muscle stretch evoked significant increases in MSNA (P < 0.005) and mean arterial blood pressure (P < 0.02). After ketorolac Bier block, passive muscle stretch did not evoke significant responses in MSNA (P = 0.11) or mean arterial blood pressure (P = 0.83). Saline Bier block had no effect on the MSNA or blood pressure response to ischemic stretch. These observations indicate that cyclooxygenase inhibition attenuates MSNA responses seen during PEMI and suggest that cyclooxygenase products sensitize the muscle mechanoreceptors.