The survey of sexual maturity in Mugil cephalus so measuring sex hormones and histologic studies

In this study the process of female gray mullet brooders was carried out by using histological study and masurment of sex steroids. Results of histological studies showed that oocyte of gray mullet brooders in Gomishan Rearing Center conditions of develop to the end of yolk globule stage. The results were observed with oocyte in chromatin nucleolar stage (first stage) with means of diameter of 20 p m, in August, perinucleolar stage (second stage) in September with mean diameter of 87 p m, yolk vesicle stage (third stage) in October with mean diameter 200 p m and yolk granules stage (forth stage) from October to November with average diameter of 180 — 650 p m. For the reason of stopping oocyte develop at the end of fourth stage, hormonal induction to final oocyte maturation and ovulation was used. For this purpose, carp pituitary , HCG and LRH-A2 with different combinations were used in two stages, second injection was used 24 hours after first injection. 15 females brooders were divided in 5 groups, different hormonal combinations were injected to four groups and to fifth group as control, only saline, was injected. The process of female brooder rippening in hormonal induction was studied via masurment of sex steroids including 17 a - hydroxy progestrone, estradio1-17)6 and testosterone. Blood samples were collected from caudal vein during first injection, 24, 30 and 48 hours after the first injection. At the same time, for distinguishing histological changes the sample has been attained from the gonads Sex stroid fluctuation patterns in different brooder groups that injected hormon were similar, however hormonal composition had similar effects. All brooder that their oocyte in the beginning of hormonal injection were At the end of fourth stage with oocyte diameter average of 600 p m received to final maturation and ovulation. The brooder that its oocytes were At the begining or mid-fourth stage did not show ovulation but hormonal induction caused oocyte develop at the beginning of fifth stage. Study of 17-hydroxy progestrone fluctuation showed that the maximum level of this steroid (0.347 ng/ml) measured 30 hours after the first injection and was significantly higher (p< 0.05) than those of control group. So, 17-hydroxy progestrone is probably precursor of maturation inducing steroid (MIS). However the maximum level of that observed was coincident with germinal vesicle breakdown, oil droplets coalescence and dissolution of yolk granuls The maximum levels of esteradiol— 17/0 and testosterone (3.778 and 16.801ng/ml,respectively) in spawned brooders,were observed 24 hours after the first injection. levels of those steroids were significantly higher (p<0.05) than control group. Maximum level of sex steroids in the brooders that did not spawn to the end of treatment was observed with more delay than those in spawned brooders. Therefor maximum level of 17a-hydroxy progestrone (0.264 ng/ml) in those brooders observed in fourth sampling time and the maximum levels of estradio1-17a and testosterone (2.944 and 18.993 ng/ml, respectivly)observed in third sampling time that was significantly higher (p<0.05) than those of control group. For the study of stress effect on brooders during the hormonal induction, level of cortisol was measured in every sampling time. level of cortisol had high fluctuation that showed handling level and stress effect on brooders. However maximum level of cortisol in majority of brooders was dominant in third sampling time that was coincident with final maturation.

Changes in plasma thyroid hormones and cortisol levels in crucian carp (Carassius auratus) exposed to the extracted microcystins

The endocrine response of crucian carp injected intraperitoneally with extracted microcystins (MC) was investigated in this study. Fish were injected intraperitoneally either with 0.75% NaCl (control) and Microcystis extract corresponding to 150 and 600 mu g microcystins per kg body weight. The plasma levels of triiodothyronine (T-3), thyroxine (T-4), free triiodothyronine (FT3), free thyroxine (FT4), and cortisol were determined at 0, 1, 3, 12, 24. and 48 h post-administration of MC-containing extract. Treated fish displayed abnormal behaviors, Such as a startle response and disoriented swimming, as well as changes in ventilation rates. Plasma cortisol concentrations of fish in both dose groups significantly increased after administration of extracted MC and remained high throughout the experiment, which suggested that MC elicited a stress response in treated fish. The profiles of cortisol changes in treated fish appeared to be dose dependent, indicating that fish in the high dose group experienced greater MC-incluced disturbance. Mortality occurred after 12 h in the high dose group. Plasma levels of T-4, T-3, FT4, and FT3 did not vary significantly between the control fish. In contrast to this, fish exposed to MC-containing extract showed significant declines in T-3, FT4, and FT3 levels in a dose-depenclent manner throughout the experiment. Plasma T4 levels, however, did not vary significantly in the low dose group, whereas they decreased significantly it 48 h post injection in the high dose group. This study demonstrates that administration of microcystins-containing extract causes a stress response and reduces the plasma levels of thyroid hormones in crucian carp. These results illustrate that microcystins exerted potent effects on the endocrine system of crucian carp, through activating their hypothalamus-pituitary- interrenal axis and disturbing thyroid function. (c) 2008 Elsevier Ltd. All rights reserved.

Evaluation of sex specificity on oxidative stress induced in lungs of mice irradiated by C-12(6+) ions

The aim of this work is to identify if there is sex specificity on C-12(6+) ion-induced oxidative damage in mouse lung at different time points. Kun-Ming mice were divided into two groups, each composed of six males and six females: control group and irradiation group with a single acute dose of 4 Gy. Animals were sacrificed at 2, 4 and 12 h respectively, there lungs were removed immediately, and the oxidative stress-related biomarkers were measured by Diagnostic Reagent Kits. The results showed that the relative activities of superoxide dismutase (4 h), catalase (2 h) and Se-dependent glutathione peroxidase (12 h) have significant changes (P < 0.05) between male groups and female groups, suggesting that the lungs of male mice are more sensitive to counteracting the oxidative challenge. Moreover, higher levels of malondiadehyde and lower contents of glutathione were also found in males, indicating that oxidative stress induced by C-12(6+) ion is pronounced in the lungs of males. We thought that these sex-responded differences may be attributed to the influence of sex hormones.

Stress-induced visceral pain in rodents: neurochemical, hormonal, immune and epigenetic mechanisms

Visceral pain is a debilitating disorder which affects up to 25% of the population at any one time. It is a global term used to describe pain originating from the internal organs, which is distinct from somatic pain. Currently the treatment strategies are unsatisfactory, with development of novel therapeutics hindered by a lack of detailed knowledge of the underlying mechanisms. The work presented in this thesis aimed to redress this issue and look in more detail at the molecular mechanisms of visceral pain in preclinical models. Stress has long been implicated in the pathophysiology of visceral pain in both preclinical and clinical studies. Here a mouse model of early-life stress-induced visceral hypersensitivity was validated. Moreover, mouse strain differences were also apparent in visceral sensitivity suggesting a possible genetic component to the underlying pathophysiology. Furthermore, gender and sex hormones were also implicated in stress sensitivity and visceral pain. Using the rat model of maternal separation, some of the epigenetic mechanisms underpinning visceral hypersensitivity, specifically the contribution of histone acetylation were unravelled. Glutamate has been well established in somatic pain processing, however, its contribution to visceral pain has not been extensively characterised. It was found that glutamate uptake is impaired in viscerally hypersensitive animals, an effect which could be reversed by treatment with riluzole, a glutamate uptake activator. Moreover, negative modulation of the metabotropic glutamate (mGlu) receptor 7 was sufficient to reverse visceral hypersensitivity in a stress sensitive rat strain, the Wistar Kyoto rat. Furthermore, toll-like receptor 4 (TLR4) was implicated in chronic stress-induced visceral hypersensitivity. Taken together, these findings have furthered our knowledge of the pathophysiology of visceral pain. In addition, we have identified glutamate transporters, mGlu7 receptor, histone acetylation and TLR4 as novel targets, amenable to pharmacological manipulation for the specific treatment of visceral pain.

Do persistent organic pollutants interact with the stress response? Individual compounds, and their mixtures, interaction with the glucocorticoid receptor

Persistent organic pollutants (POPs) are toxic substances, highly resistant to environmental degradation, which can bio-accumulate and have long-range atmospheric transport potential (UNEP 2001). The majority of studies on endocrine disruption have focused on interferences on the sexual steroid hormones and so have overlooked disruption to glucocorticoid hormones. Here the endocrine disrupting potential of individual POPs and their mixtures has been investigated in vitro to identify any disruption to glucocorticoid nuclear receptor transcriptional activity. POP mixtures were screened for glucocorticoid receptor (GR) translocation using a GR redistribution assay (RA) on a CellInsight(TM) NXT High Content Screening (HCS) platform. A mammalian reporter gene assay (RGA) was then used to assess the individual POPs, and their mixtures, for effects on glucocorticoid nuclear receptor transactivation. POP mixtures did not induce GR translocation in the GR RA or produce an agonist response in the GR RGA. However, in the antagonist test, in the presence of cortisol, an individual POP, p,p'-dichlorodiphenyldichloroethylene (DDE), was found to decrease glucocorticoid nuclear receptor transcriptional activity to 72.5% (in comparison to the positive cortisol control). Enhanced nuclear transcriptional activity, in the presence of cortisol, was evident for the two lowest concentrations of perfluorodecanoic acid (PFOS) potassium salt (0.0147mg/ml and 0.0294mg/ml), the two highest concentrations of perfluorodecanoic acid (PFDA) (0.0025mg/ml and 0.005mg/ml) and the highest concentration of 2,2',4,4'-tetrabromodiphenyl ether (BDE 47) (0.0000858mg/ml). It is important to gain a better understanding of how POPs can interact with GRs as the disruption of glucocorticoid action is thought to contribute to complex diseases.

Impact du stress sur la survie des lymphocytes T CD8+ mémoires dans le contexte des missions spatiales.

La mémoire immunitaire permet à l’organisme de se souvenir de tous les agents pathogènes rencontrés afin de pouvoir monter une réponse immunitaire plus rapide et plus efficace en cas de réinfection. Après la phase de contraction de la réponse primaire, les lymphocytes T CD8 mémoires survivent grâce à la présence de cytokines telle que l’interleukine 15 (IL-15). Ces cellules permettent aussi au système immunitaire de contrôler les virus latents n’ayant pas été totalement éliminés de l’hôte. Les situations de stress chronique affectent le système immunitaire provoquant la réactivation des virus latents. Des titres viraux élevés de virus de la famille Herspeviridea ont été observés chez les astronautes à leur retour de mission, suggérant que les hormones libérées en situation de stress auraient un impact négatif sur les lymphocytes T CD8+ mémoires. Un modèle de stress chronique in vitro chez la souris a été élaboré en ajoutant de la corticostérone à des lymphocytes T CD8+ mémoires. Il a ainsi été démontré que l’hormone de stress avait un effet pro-apoptotique sur ces cellules et que cet effet était partiellement inhibé par l’IL-15. Des cibles moléculaires ont aussi été identifiées afin de suivre la fonction immunitaire mémoire lors des vols spatiaux à l’aide du cytomètre en flux Microflow1, une nouvelle plateforme portative de diagnostic biomédical. Les résultats des tests en laboratoire puis dans la Station Spatiale Internationale (SSI) démontrent qu’il sera possible de suivre la fonction immunitaire mémoire et les marqueurs de stress en temps réel lors des vols spatiaux.

Reactive oxygen and nitrogen species balance in the determination of thyroid hormones-induced cardiac hypertrophy mediated by renin-angiotensin system

Role of reactive oxygen species (ROS)/nitric oxide (NO) balance and renin-angiotensin system in mediating cardiac hypertrophy in hyperthyroidism was evaluated in an in vivo and in vitro experimental model. Male Wistar rats were divided into four groups: control, thyroid hormone, vitamin E (or Trolox, its hydrosoluble analogue), thyroid hormone + vitamin E. Angiotensin II receptor (AT1/AT2) gene expression, immunocontent of AT1/AT2 receptors, angiotensinogen, NADPH oxidase (Nox2), and nitric oxide synthase isoforms, as well as ROS concentration (hydrogen peroxide and superoxide anion) were quantified in myocardium. Thyroid hormone increased ROS and NO metabolites, iNOS, nNOS and eNOS isoforms and it was accompanied by cardiac hypertrophy. AT1/AT2 expression and the immunocontent of angiotensinogen and Nox2 were enhanced by thyroid hormone. Antioxidants reduced ROS levels, Nox2, AT1/AT2, NOS isoforms and cardiac hypertrophy. In conclusion, ROS/NO balance may play a role in the control of thyroid hormone-induced cardiac hypertrophy mediated by renin-angiotensin system. (C) 2011 Elsevier Ireland Ltd. All rights reserved.

Testosterone suppresses oxidative stress in human neutrophils

The in vitro effect of testosterone on human neutrophil function was investigated. Blood neutrophils from healthy male subjects were isolated and treated with 10 nM, 0.1 and 10 mu M testosterone for 24 h. As compared with untreated cells, the testosterone treatment produced a significant decrease of superoxide production as indicated by the measurement of extra- and intracellular superoxide content. An increment in the production of nitric oxide was observed at 0.1 and 10 mu M testosterone concentrations, whereas no effect was found for 10 nM. Intracellular calcium mobilization was significantly increased at 10 nM, whereas it was reduced at 10 mu M testosterone. There was an increase in phagocytic capacity at 10 nM and a decrease of microbicidal activity in neutrophils treated with testosterone at 10 mu M. Glutathione reductase activity was increased by testosterone treatment, whereas no effect was observed in other antioxidant enzyme activities. An increase in the content of thiol groups was observed at all testosterone concentrations. Lipid peroxidation in neutrophils evaluated by levels of TBARS was decreased at 10 nM and 0.1 mu M testosterone. These results indicate the antioxidant properties of testosterone in neutrophils as suggested by reduction of superoxide anion production, and lipid peroxidation, and by the increase in nitric oxide production, glutathione reductase activity and the content of thiol groups. Therefore, the plasma levels of testosterone are important regulators of neutrophil function and so of the inflammatory response. Copyright (C) 2010 John Wiley & Sons, Ltd.

Relationship between stress, eating behavior and obesity

Stress is thought to influence human eating behavior and has been examined in animal and human studies. Our understanding of the stress-eating relation is confounded by limitations inherent in the study designs; however, we can make some tentative conclusions that support the notion that stress can influence eating patterns in humans. Stress appears to alter overall food intake in two ways, resulting in under- or overeating, which may be influenced by stressor severity. Chronic life stress seems to be associated with a greater preference for energy- and nutrient-dense foods, namely those that are high in sugar and fat. Evidence from longitudinal studies suggests that chronic life stress may be causally linked to weight gain, with a greater effect seen in men. Stress-induced eating may be one factor contributing to the development of obesity. Future studies that measure biological markers of stress will assist our understanding of the physiologic mechanism underlying the stress-eating relation and how stress might be linked to neurotransmitters and hormones that control appetite.

Maternal stress to partner quality is linked to adaptive offspring sex ratio adjustment

Female birds have been shown to have a remarkable degree of control over the sex ratio of the offspring they produce. However, it remains poorly understood how these skews are achieved. Female condition, and consequent variation in circulating hormones, provides a plausible mechanistic link between offspring sex biases and the environmental and social stresses commonly invoked to explain adaptive sex allocation, such as diet, territory quality, and body condition. However, although experimental studies have shown that female perception of male phenotype alone can lead to sex ratio biases, it is unknown how partner quality influences female physiological state. Using a controlled within-female experimental design where female Gouldian finches (Erythrura gouldiae) bred with both high- and low-quality males, we found that partner quality directly affects female hormonal status and subsequent fitness. When constrained to breeding with low-quality males, females had highly elevated stress responses (corticosterone levels) and produced adaptive male-biased sex ratios, whereas when they bred with high-quality males, females had low corticosterone levels and produced an equal offspring sex ratio. There was no effect of other maternal hormones (e.g., testosterone) or body condition on offspring sex ratios. Female physiological condition during egg production, and variation in circulating hormones in particular, may provide a general mechanistic route for strategic sex allocation in birds.

Covariation in life-history traits : differential effects of diet on condition, hormones, behavior, and reproduction in genetic finch morphs

The relative contribution of genetic and environmental factors in determining variation in life-history traits is of central interest to evolutionary biologists, but the physiological mechanisms underlying these traits are still poorly understood. Here we experimentally demonstrate opposing effects of nutritional stress on immune function, endocrine physiology, parental care, and reproduction between red and black head-color morphs of the Gouldian finch (Erythrura gouldiae). Although the body condition of black morphs was largely unaffected by diet manipulation, red birds were highly sensitive to dietary changes, exhibiting considerable within-individual changes in condition and immune function. Consequently, nutritionally stressed red birds delayed breeding, produced smaller broods, and reared fewer and lower-quality foster offspring than black morphs. Differences in offspring quality were largely due to morph-specific differences in parental effort: red morphs reduced parental provisioning, whereas black morphs adaptively elevated their provisioning effort to meet the increased nutritional demands of their foster brood. Nutritionally stressed genetic morphs also exhibited divergent glucocorticoid responses. Black morphs showed reduced corticosterone-binding globulin (CBG) concentrations and increased levels of free corticosterone, whereas red morphs exhibited reduced free corticosterone levels and elevated CBG concentrations. These opposing glucocorticoid responses highlight intrinsic differences in endocrine sensitivities and plasticity between genetic morphs, which may underlie the morph-specific differences in condition, behavior, and reproduction and thus ultimately contribute to the evolution and maintenance of color polymorphism.

Increased Biomass, Seed Yield and Stress Tolerance Is Conferred in Arabidopsis by a Novel Enzyme from the Resurrection Grass Sporobolus stapfianus That Glycosylates the Strigolactone Analogue GR24

Isolation of gene transcripts from desiccated leaf tissues of the resurrection grass, Sporobolus stapfianus, resulted in the identification of a gene, SDG8i, encoding a Group 1 glycosyltransferase (UGT). Here, we examine the effects of introducing this gene, under control of the CaMV35S promoter, into the model plant Arabidopsis thaliana. Results show that Arabidopsis plants constitutively over-expressing SDG8i exhibit enhanced growth, reduced senescence, cold tolerance and a substantial improvement in protoplasmic drought tolerance. We hypothesise that expression of SDG8i in Arabidopsis negatively affects the bioactivity of metabolite/s that mediate/s environmentally-induced repression of cell division and expansion, both during normal development and in response to stress. The phenotype of transgenic plants over-expressing SDG8i suggests modulation in activities of both growth- and stress-related hormones. Plants overexpressing the UGT show evidence of elevated auxin levels, with the enzyme acting downstream of ABA to reduce drought-induced senescence. Analysis of the in vitro activity of the UGT recombinant protein product demonstrates that SDG8i can glycosylate the synthetic strigolactone analogue GR24, evoking a link with strigolactone-related processes in vivo. The large improvements observed in survival of transgenic Arabidopsis plants under cold-, salt- and drought-stress, as well as the substantial increases in growth rate and seed yield under non-stress conditions, indicates that overexpression of SDG8i in crop plants may provide a novel means of increasing plant productivity.

Susceptibility of reproduction in female pigs to impairment by stress and the role of the hypothalamo-pituitary-adrenal axis

Although it is generally considered that stress can impair reproduction, we suggest that the impact of acute or repeated acute stress or acute or repeated acute elevations of cortisol are of little consequence in female pigs, even if these occur during the series of endocrine events that induce oestrus and ovulation. It is important to understand the impact of acute stress on reproduction because, in the intensive production of livestock, animals are often subjected to short-term challenges. There seems little doubt that reproduction in a proportion of female pigs is susceptible to impairment by severe and prolonged stress or the sustained elevation of cortisol but only when this continues for a substantial period. In female pigs, where reproduction is susceptible to impairment by severe prolonged stress, it is possible that the mediators of this suppression are cortisol, corticotrophin-releasing factor and vasopressin but, in pigs, there is evidence to suggest that adrenocorticotrophic hormone is not involved. Other substances secreted during stress may be involved but these are not considered in this review. It is possible that the mediators of stress act at any level of the hypothalamo-pituitary-ovarian axis. Although a variety of experimental manipulations have provided potential mediators and mechanisms for the stress-induced suppression of reproduction, these experimental manipulations rarely represented physiological circumstances so it is not clear if such mechanisms would be important in a physiological context. The precise mediators and mechanisms by which hormones released during stress may inhibit reproductive processes during severe prolonged stress are yet to be determined.

Adrenocortical stress responses influence an invasive vertebrate's fitness in an extreme environment

Continued range expansion into physiologically challenging environments requires invasive species to maintain adaptive phenotypic performance. The adrenocortical stress response, governed in part by glucocorticoid hormones, influences physiological and behavioural responses of vertebrates to environmental stressors. However, any adaptive role of this response in invasive populations that are expanding into extreme environments is currently unclear. We experimentally manipulated the adrenocortical stress response of invasive cane toads (Rhinella marina) to investigate its effect on phenotypic performance and fitness at the species' range front in the Tanami Desert, Australia. Here, toads are vulnerable to overheating and dehydration during the annual hot-dry season and display elevated plasma corticosterone levels indicative of severe environmental stress. By comparing unmanipulated control toads with toads whose adrenocortical stress response was manipulated to increase acute physiological stress responsiveness, we found that control toads had significantly reduced daily evaporative water loss and higher survival relative to the experimental animals. The adrenocortical stress response hence appears essential in facilitating complex phenotypic performance and setting fitness trajectories of individuals from invasive species during range expansion.

The effect of elevated blood cortisol levels on the extinction of a conditioned stress response in rainbow trout

Following previously published observations that a conditioned response (CR) was lost more quickly by rainbow trout (Oncorhynchus mykiss) exhibiting a high responsiveness to stressors than by low responding individuals this study was designed to investigate the effects of exogenous cortisol on the retention of a CR in unselected rainbow trout. Fish held in isolation were conditioned over a 10-day period by pairing an innocuous signal (conditioned stimulus, CS: a water jet played on the surface of the tank water) with a mild stressor (unconditioned stimulus, US: 30 min of confinement). This resulted in a brief elevation of plasma cortisol levels (the CR) when the fish was exposed to the CS only. The effect of exogenous cortisol on the retention of the CR was evaluated by comparing the performance of fish that received cortisol-containing slow-release intraperitoneal implants, with fish receiving vehicle-only implants. Retention of the CR was assessed at intervals up to 35 days after conditioning ceased. The CR was considered to be evident when 30 min following presentation of the CS, mean plasma cortisol levels were significantly higher in conditioned than untrained fish. on day 1 both cortisol-implanted and vehicle-implanted conditioned fish exhibited a CR. However, from day 5 onwards the CR was observed only in the vehicle-implanted and conditioned group. This finding indicates that administration of cortisol accelerated the extinction of the CR in the cortisol-implanted fish, suggesting that elevated plasma cortisol levels can impair memory processes in rainbow trout. (c) 2006 Elsevier B.V. All rights reserved.