Deciphering the mechanisms involving cenexin, ninein and centriolin in sperm maturation during epididymal transit in the domestic cat.

The sperm centrosome is an essential organelle with a key role in organizing the sperm aster for proper syngamy and formation of the first mitotic spindle. The sperm cell acquires the functional capability during epididymal transit by incorporation of key factors. The objective of the study was to identify these key maturation proteins, such as ninein and centriolin as well as cenexin-a scaffold protein that serves to bind ninein and centriolin. Epididymal samples were dissected from 17 adult cat testes (>1 year old) and spermatozoa were extracted from the different regions, including rete testis, caput, corpus, cauda and vas deferens. Tissue samples and sperm cells were fixed separately in 4% paraformaldehyde before immunostaining with anticenexin, ninein or centriolin antibodies. Results showed that the proportion of sperm cells with cenexin localized at the centrosome progressively increased along the tract with the lowest percentage of stained cells in the testis (mean = 45%) and highest in the cauda (mean = 81%). Although not significant, the intensity of cenexin immunofluorescence in positive cells increased twofold from the testis to vas deferens. There was no significant difference in the proportion of sperm labelled with centriolin or ninein (ranges of 21%-26% and 33%-48% between segments, respectively) or the intensity (±58% and ±63% change as compared to testis, respectively). Cenexin may serve as a scaffold protein for centriolin and ninein, as the vast majority of spermatozoa only displayed colocalization of these proteins when cenexin was also present (mean = 85% and 91% colocalization, respectively). In summary, these results could be applied to future efforts to create an in vitro culture system capable of rescuing the impaired centrosome of an infertile male, with particular potential for wild felid conservation.

SU-E-T-309: Dosimetric Study and Clinical Implementation of an HDR Applicator of SAVI for Partial Breast Irradiation.

PURPOSE: To present clinical implementation and quality assurance for a new HDR applicator of Strut-Adjusted Volume Implant (SAVI) for partial breast irradiation and the higher-order DVH examined. METHODS: The SAVI applicator with multi-peripheral struts can be differentially loaded with the HDR source for a conformal dose distribution to the lumpectomy cavity. The treatment plan is evaluated by a dose volume histogram (DVH) as follows: V90 > 90%, V150 < 50 cc, and V200 < 20 cc. A higher-order DVH which may reflect radiation-induced toxicity, such as V300, was studied. The SAVI device status was verified by the 3D CT images and image fusion. Tissue invagination was investigated using an ion chamber and film with the cavity filled with air and water merged into a water phantom. RESULTS: Twenty-nine patients to date at Mercy Medical Center, Baltimore, Maryland were treated with SAVI device. The dosimetric data demonstrated the achievements of greater than 90% coverage for V90 at 96.8% and 94.1% for V95 while keeping a low V150 at 33.9 cc and V200 at 16.5 cc. V300 was found to be 2.7 cc in average. Potential uncertainties introduced by the SAVI applicator motion were a 3% variation in dose caused either by a 3-mm} translation or a rotation of 3 degree. CONCLUSIONS: Multiple catheters of the SAVI applicator allows for optimal and conformal dose distribution around a lumpectomy cavity while minimizing the dose to adjacent normal structures such as skin and ribcage. Multiple imaging techniques are capable to verify cavity variation, strut collapse or relative motion, and device shift. A nearly fully loaded dwell source position produced the discrepancy of less than 3% and allow for optimal and conformal dose distribution to a lumpectomy cavity. Advantages of the SAVI applicator have been shown in treating breast cancer with the shallower, elliptical, and asymmetric cavity.

Oral progestin induces rapid, reversible suppression of ovarian activity in the cat.

The influence of oral progestin (altrenogest; ALT) on cat ovarian activity was studied using non-invasive fecal steroid monitoring. Queens were assigned to various ALT dosages: (1) 0mg/kg (control; n=5 cats); (2) 0.044 mg/kg (LOW; n=5); (3) 0.088 mg/kg (MID; n=6); or (4) 0.352 mg/kg (HIGH; n=6). Fecal estrogen and progestagen concentrations were quantified using enzyme immunoassays for 60 days before, 38 days during and 60 days after ALT treatment. Initiation of follicular activity was suppressed in all cats during progestin treatment, whereas controls continued to cycle normally. Females (n=6) with elevated fecal estrogens at treatment onset completed a normal follicular phase before returning to baseline and remained suppressed until treatment withdrawal. All cats receiving oral progestin re-initiated follicular activity after treatment, although MID cats experienced the most synchronized return (within 10-16 days). Mean baseline fecal estrogens and progestagens were higher (P<0.05) after treatment in HIGH, but not in LOW or MID cats compared to pre-treatment values. The results demonstrate that: (1) oral progestin rapidly suppresses initiation of follicular activity in the cat, but does not influence a follicular phase that exists before treatment initiation; and (2) queens return to normal follicular activity after progestin withdrawal. This study provides foundational information for research aimed at using progestin priming to improve ovarian response in felids scheduled for ovulation induction and assisted breeding.

Effects of xenoestrogens on the differentiation of behaviorally-relevant neural circuits.

It has become increasingly clear that environmental chemicals have the capability of impacting endocrine function. Moreover, these endocrine disrupting chemicals (EDCs) have long term consequences on adult reproductive function, especially if exposure occurs during embryonic development thereby affecting sexual differentiation. Of the EDCs, most of the research has been conducted on the effects of estrogen active compounds. Although androgen active compounds are also present in the environment, much less information is available about their action. However, in the case of xenoestrogens, there is mounting evidence for long-term consequences of early exposure at a range of doses. In this review, we present data relative to two widely used animal models: the mouse and the Japanese quail. These two species long have been used to understand neural, neuroendocrine, and behavioral components of reproduction and are therefore optimal models to understand how these components are altered by precocious exposure to EDCs. In particular we discuss effects of bisphenol A and methoxychlor on the dopaminergic and noradrenergic systems in rodents and the impact of these alterations. In addition, the effects of embryonic exposure to diethylstilbestrol, genistein or ethylene,1,1-dichloro-2,2-bis(p-chlorophenyl) is reviewed relative to behavioral impairment and associated alterations in the sexually dimorphic parvocellular vasotocin system in quail. We point out how sexually dimorphic behaviors are particularly useful to verify adverse developmental consequences produced by chemicals with endocrine disrupting properties, by examining either reproductive or non-reproductive behaviors.

Neuroendocrine and immune characteristics of aging in avian species.

Avian species show a remarkable diversity in lifespan. The differing lifespan patterns are found across a number of birds, in spite of higher body temperature and apparent increased metabolic rate. These characteristics make study of age-related changes of great interest, especially for understanding the biology of aging associated with surprisingly long lifespan in some birds. Our studies have focused on a short-lived avian model, the Japanese quail in order to describe reproductive aging and the neuroendocrine characteristics leading to reproductive senescence. Biomarkers of aging used in mammalian species include telomere length, oxidative damage, and selected metabolic indicators. These markers provide confirming evidence that the long-lived birds appear to age more slowly. A corollary area of interest is that of immune function and aging. Immune responses have been studied in selected wild birds and there has been a range of studies that have considered the effects of stress in wild and domestic species. Our laboratory studies have specifically tested response to immune challenge relative to aging in the quail model and these studies indicate that there is an age-related change in the qualitative aspects of the response. However, there are also intriguing differences in the ability of the aging quail to respond that differ from mammalian data. Finally, another approach to understanding aging is to attempt to develop or test strategies that may extend lifespan and presumably health. One area of great interest has been to consider the effect of calorie restriction, which is a treatment shown to extend lifespan in a variety of species. This approach is routinely used in domestic poultry as a means for extending reproductive function and enhancing health. Our data indicate that moderate calorie restriction has beneficial effects, and that physiological and endocrine responses reflect these benefits.

Reproductive aging in Japanese quail, Coturnix japonica is associated with changes in central opioid receptors.

Quantitative in vitro autoradiography was used to measure specific mu and delta opioid receptor densities in regions of the Japanese quail, Coturnix japonica, brain that regulates reproductive endocrine and behavioral responses to determine the possible involvement of the opioid system in reproductive decline seen during aging. Densities were measured in selected brain regions of young sexually active (YAM), young photoregressed (YPM), old reproductively senescent (OIM) male, young active (YF), and old senescent female (OF) Japanese quail. Medial and lateral septum (SM, SL), medial preoptic area (POM), and n. intercollicularis (ICo) were of particular interest for reproductive responses. Similar to previous observations, mu and delta opioid receptors showed differential distributions in the areas measured. Some age-related changes were observed, with lower SM mu receptor densities in aged males (OIM) than females or young males (YAM). Densities of mu receptors in the POM and in other areas examined did not vary with sex or age. Similarly, OIM males had lower densities of delta receptors in the SM than young males (YAM and YPM); POM delta receptor densities were also low in OIM males compared to the YPM males, and YAM males were intermediate. Interestingly, photoregressed males (YPM) had higher SL delta receptor densities than any other group. Thus there were age-related differences detected in mu receptor densities among groups in the SM of OIM relative to other groups; and the mu and delta receptor densities did not differ in females with brain region. Additionally for delta receptors specifically, YF and OF did not differ from OIM for any brain region and similarly had lower densities of delta receptors compared to YAM males. These data provide support for regional differences in opioid receptor distribution and for age- and sex-related differences in delta opioid receptor densities. The direction of change presents an interesting dichotomy in that, compared to young active males, delta opioid receptor densities increased with loss of reproductive function in the YPM, whereas receptor densities decreased in the OIM. Plasma androgen levels were relatively low in both these groups compared to the young active males. This observation suggests that there is an age-related loss in the ability of this receptor system to respond to circulating and centrally produced steroid hormones in the POM and in some septal regions, compared to young animals that are responding to environmental cues. Furthermore, these data support an active role of the opioid peptide system in the inhibition of the reproductive axis in photoregression.

Can testosterone and corticosterone predict the rate of display of male sexual behaviour, development of secondary sexual characters and fertility potential in primary broiler breeders?

1. Genetic selection for growth to enhance production may be associated with stress and with modified physiological and behavioural phenotypes which depress male primary broiler breeder fertility. 2. We hypothesised that male serum testosterone (T) and corticosterone (C) concentrations might correlate with fertility, sexual behaviour, and testicular, comb and wattle size. 3. Cockerels from two genetic strains (A and B) of primary broiler breeder were penned individually with an average of 10 females across 5 age periods (30 to 51 weeks) to evaluate male fertility, behaviour, serum T and C, and comb, wattle and testicular dimensions. 4. Strain A males had higher T at age periods 2, 4 and 5 than Strain B. Both strains had basal concentrations of C, apart from an elevated concentration for Strain B in period 5. 5. Strain B had a weak but significant, positive correlation between sexual behaviour and T and C, while Strain A males with higher C had larger combs and wattles. 6. Neither T nor C correlated with fertility. We conclude that evaluation of these endocrine factors (quantifiable measurements with the potential to correlate with fertility) alone seems insufficient to predict male fertility potential in these strains of primary broiler breeder.

Fluctuating asymmetry and growth as biomarkers for exposure to androgen disrupting chemicals in Japanese quail.

The effects of embryonic exposure to androgen disrupting chemicals (ADCs) on growth and fluctuating asymmetry (FA) were determined in Japanese quail chicks. Embryos were exposed to an anti-androgenic chemical, 1,1,1-Trichloro-2,2-bis(p-chlorophenyl)ethane (p,p'-DDE) at 20 or 40 microg, or to an androgenic chemical, trenbolone acetate, at 5 or 50 microg on day one of incubation. Growth was measured by body weight and tarsus and culmen lengths from day of hatch until day 29. FA was measured as differences in right versus left lengths of the tarsus, radius, zygomatic process, and premaxilla in day old carcasses. No differences in FA were observed for either treatment. Embryonic exposure to DDE resulted in no significant differences in all measures of growth, although the same quail exhibited significant differences in immunological, reproductive, and behavioral measurements (reported elsewhere). Chicks exposed to trenbolone exhibited no differences in body weight or measures of FA at day of hatch, however, subsequent growth was inhibited. This study shows that although growth and FA are often used as measures of chemical stress experienced during embryonic development, they are not sensitive measures for exposure to these ADCs at these levels in Japanese quail.

Consequences of endocrine disrupting chemicals on reproductive endocrine function in birds: establishing reliable end points of exposure.

It has been difficult to establish reliable indices of exposure to endocrine disrupting chemicals (EDCs) appropriate for a variety of avian species because of a vast array of reproductive strategies. Data from mammals, reptiles and fish provide insight on likely mechanisms of action for EDCs. However, many of the effects of EDCs are weaker than the actions of the native hormones, making it difficult to assess adverse effects in domestic and wild birds. It is clear that differential sensitivity to EDCs exists across species, due to the timing and mode of exposure, compound toxicity and age of the individual. Our studies on EDCs are conducted in the quail model system, with focus on reproductive endocrine, neuroendocrine and behavioral responses. Studies have included EDC exposure, either by egg injection or via diet. Results from egg injection studies showed the following: (1) estradiol administered by embryonic day 12 demasculinized male sexual behavior, altered hypothalamic neurotransmitters and reduced hen day production and fertility in a dose dependent fashion, (2) methoxychlor (MXC) or vinclozolin impaired male sexual behavior in adult quail and (3) DDE exposure impaired reproductive and immune related end points. Two-generation studies were conducted on Japanese and northern bobwhite quail with dietary methoxychlor (MXC) exposure (0, 5 and 10 ppm) beginning in adults (P1), continuing in their offspring (F1), with F2 offspring raised on control diet. MXC exposure impaired male sexual behavior, hypothalamic catecholamines and plasma steroid hormones. Moreover, MXC exposure had reproductive consequences observable at both the lower and higher doses of MXC in F1 and F2 generations. These data demonstrate that embryonic EDC exposure interferes with sexual differentiation of neural systems that direct reproduction.

Short term suppression of follicular recruitment and spontaneous ovulation in the cat using levonorgestrel versus a GnRH antagonist.

Suppression and subsequent rebound of ovarian activity using a progestin (levonorgestrel; Norplant) versus a GnRH antagonist (antide) was assessed in the domestic cat via fecal estradiol and progesterone metabolite analyses. Following an initial dose-response trial, queens were assigned to one of four treatments: (1) antide, two 6 mg/kg injections 15 days apart (n = 8 cats); (2) levonorgestrel, six silastic rods (36 mg levonorgestrel/rod) implanted for 30 days (n = 8); (3) control injections (n = 5); and (4) control implants (n = 5). Steroid metabolites were quantified from daily fecal samples for 90 days before, 30 days during, and 90 days after treatment. Antide and levonorgestrel inhibited estrous cyclicity in contrast to continued cyclicity in controls. Cats already at estradiol baseline in antide (n = 7) and levonorgestrel (n = 4) groups remained inhibited during treatment. In females with elevated estradiol levels at treatment onset (Day 0), a normal estradiol surge was completed before concentrations declined to baseline (approximately Days 5-7) and remained suppressed throughout the remaining treatment period. Additionally, 56% of treatment animals exhibited at least one spontaneous ovulation during the pre-treatment period, but no female ovulated during treatment with levonorgestrel or antide. Antide-treated cats exhibited lower (P < 0.05) baseline estradiol concentrations during treatment compared to pre- and post-treatment. In contrast, levonorgestrel induced elevations in baseline estradiol following treatment compared to pre- and during treatment intervals. Control females showed no change (P > 0.05) in baseline estradiol throughout the study period. All levonorgestrel and antide cats returned to estrus after treatment withdrawal. Results demonstrate that: (1) both antide and levonorgestrel are effective for inducing short-term suppression of follicular recruitment and ovulation in the cat; (2) inhibition is reversible; and (3) GnRH antagonists and progestins differentially regulate basal estradiol secretion. This study also confirmed a relatively high incidence of spontaneous ovulation in the cat, a species generally considered to be an induced ovulator.

Introduction: neurobiological impact of environmental estrogens.

This paper provides an introduction to a special issue dedicated to the action of environmental estrogens on neural circuits and behavior. The problem of endocrine disrupting chemicals (EDCs), i.e. chemicals that have the capacity to interfere with the endocrine system, has gained increasing attention as it has become clear that these environmental contaminants may be active in humans, as well as in wildlife and domestic animal species. The majority of the early investigations were aimed at the discovery of the toxicological effects of the EDCs, but biomedical observations were among some of the first indications that estrogenic compounds may exert deleterious effects, even some time after exposure. The data derived from women exposed prenatally to diethylstilbesterol provided powerful evidence for long-term effects and endocrine disruption associated with selected compounds. The examination of wild animal populations exposed to industrial chemicals showed that the chemical exposure, though nonlethal, left the individual impaired or even incapable of reproducing. Among the multiple targets of the action of EDCs, several researches performed in recent years have investigated subtle modifications of the animal behaviors (reproductive, aggressive) that are likely to be related to alterations of specific neural pathways. We have, therefore, focused here on the behavioral studies as one of the more powerful tools to investigate EDCs effects on specific neural circuits.

Birds as long-lived animal models for the study of aging.

Despite their high lifetime energy expenditures, most birds can be characterized as long-lived homeotherms with moderately slow aging. A growing body of research confirms the prediction that birds have special adaptations for preventing aging-related oxidative and glycoxidative damage. Nonetheless, biogerontologists have been slow to develop avian laboratory models. A number of domestic poultry and cage bird species represent either established or very promising animal models for studies of basic aging processes and their prevention, including degenerative neurobiological, behavioral and reproductive processes. Several kinds of birds have also been used in studies of cellular resistance to oxidative stressors in vitro. Results of preliminary studies on chickens and quail suggest that caloric restriction may extend the reproductive life span of hens, but its long-term effects on life span remain unstudied. Birds' innate anti-aging mechanisms may actually make them more suitable in some respects as models of longevity than short-lived laboratory rodents, and bird studies may ultimately reveal routes for therapeutic intervention in diseases of human aging and infertility.

Toxicity of lead-contaminated sediment to mute swans.

Most ecotoxicological risk assessments of wildlife emphasize contaminant exposure through ingestion of food and water. However, the role of incidental ingestion of sediment-bound contaminants has not been adequately appreciated in these assessments. This study evaluates the toxicological consequences of contamination of sediments with metals from hard-rock mining and smelting activities. Lead-contaminated sediments collected from the Coeur d'Alene River Basin in Idaho were combined with either a commercial avian maintenance diet or ground rice and fed to captive mute swans (Cygnus olor) for 6 weeks. Experimental treatments consisted of maintenance or rice diets containing 0, 12 (no rice group), or 24% highly contaminated (3,950 microg/g lead) sediment or 24% reference (9.7 microg/g lead) sediment. Although none of the swans died, the group fed a rice diet containing 24% lead-contaminated sediment were the most severely affected, experiencing a 24% decrease in mean body weight, including three birds that became emaciated. All birds in this treatment group had nephrosis; abnormally dark, viscous bile; and significant (p

Cloning of a partial cDNA for Japanese quail thyroid-stimulating hormone and effects of methimazole on the thyroid and reproductive axes.

The purposes of this study were to develop a probe for the detection of thyroid-stimulating hormone (TSH) beta subunit mRNA, to validate the usefulness of that probe in measuring TSH, and to use it to investigate the effects of thyroid suppression on TSH and the reproductive axis in Japanese quail. The objectives of experiment 1 were to isolate and characterize a partial cDNA for quail TSH and validate a riboprobe transcribed from this cDNA. This riboprobe was then used to assess changes in TSHbeta mRNA levels in Japanese quail. We isolated a cDNA of 168 bp with 94% identity to the corresponding sequence in chicken TSHbeta. The transcribed riboprobe was shown to be pituitary gland specific, and differences in TSHbeta mRNA levels were detectable with 2.5 microg of total RNA in Northern blot analysis. In experiment 2, our objective was to determine if thyroid inhibition would result in a detectable change in TSHbeta mRNA and alterations in the pituitary luteinizing hormone (LH) or indices of gonadal function. We used adult, reproductively active, male Japanese quail on a long-day photoperiod. Treatment with a goitrogen, methimazole (MMI), increased (P < 0.05) thyroid gland and liver weights and decreased (P < 0.05) serum thyroxine (T4) concentrations compared to control birds. We detected increased TSHbeta mRNA in the pituitaries of MMI-treated birds compared to controls. There was no effect of MMI treatment on the reproductive variables measured, including LHbeta mRNA levels, serum androgen and estradiol concentrations, gonad weight, or cloacal gland area. Therefore, it appears that thyroid axis inhibition and the consequent increase in TSHbeta mRNA did not have direct effects on reproductive axis function in male Japanese quail.

Hypothalamic indolamines during embryonic development and effects of steroid exposure.

The serotonin system has been implicated in the modulation of endocrine and behavioral components of reproduction. In this study, we examined endogenous hypothalamic indolamines during sexual differentiation and long-term effects of exogenous steroids during this time. In Experiment 1, Japanese quail were studied during the last half of embryonic development and early post-hatch. Samples were taken at embryonic day 10 (E10), E12, E14, E16, hatch (day 0), and days 3 and 5, post-hatch. Hypothalamic indolamines, including serotonin (5-HT) and its metabolite, 5-hydroxy indole acetic acid (5-HIAA) were measured by HPLC-EC detection. Females had relatively higher hypothalamic 5-HT at E14 than males, with both sexes showing increasing levels thereafter. By day 5, post-hatch, hypothalamic 5-HT content was higher in males than in females. When turnover was estimated by comparing relative concentrations of 5-HT to 5-HIAA, males were significantly higher at E12 and E14 than females. These data suggest that there are stage specific changes in the serotonin system, as well as sexually dimorphic patterns in the ontogeny and activity of this system. In Experiment 2, we investigated the effects of embryonic steroid hormone treatment on the serotonin system and on male sexual behavior. Birds were treated with either estradiol benzoate (EB), testosterone propionate (TP) or sesame oil (vehicle control) at selected embryonic days (E10, E12, E14, E16, 0, D3, and D5). At 4 weeks post-hatch, birds were transferred to short photoperiod (16D:8L) for 3 weeks to prevent photostimulated reproductive development. At 7 weeks of age, males were implanted with a 20mm silastic capsule filled with testosterone and sexual behavior was tested 1 week later. Brains were collected from both males and females, and preoptic area (POA) indolamines were measured. Steroid treatment at E10 or E12 resulted in the loss of male sexual behavior. Moreover, males treated with EB or TP on E12 also had increased POA 5-HT content as adults, compared to control males. Females treated with EB on either E10 or E 12 also had higher POA 5-HT content than control or TP treated females. These data provide evidence for sexual dimorphism in the hypothalamic 5-HT system at specific stages during embryonic development. Moreover, males were sensitive to exogenous EB and TP on E12, whereas females appeared to be affected by EB only and appeared to be sensitive to steroid effects over a longer period of time in development. Moreover, exogenous steroids at E12 in males also correlated with impaired sexual behavioral. These data suggest that long-term effects of embryonic steroid exposure may be mediated in part through effects on the serotonin neurotransmitter system.

Effects of exogenous testosterone on testicular luteinizing hormone and follicle-stimulating hormone receptors during aging.

During aging, the male Japanese quail exhibits a loss of fertility, increased morphological abnormalities in the testes, and a higher incidence of Sertoli cell tumors. Although there is a coincident loss of reproductive behavior, plasma androgen levels remain high until testicular regression occurs in association with senescence. The purpose of this study was to compare mean specific binding of chicken luteinizing hormone (LH) and follicle-stimulating hormone (FSH) as a measure of testicular receptors during identified stages during aging. Males were categorized according to age (young = 9 months, middle aged = 24 months, or old = 36+ months) and sexual behavior (active or inactive). Testicular samples were collected immediately after perfusion with 4% paraformaldehyde from the following groups: young active (n = 8), young photoregressed (n = 5), young photoregressed plus testosterone implant (n = 4), middle-aged active (n = 8), middle-aged inactive (n = 4), old inactive (n = 5), and old inactive plus testosterone implant (n = 6). A crude plasma membrane fraction was prepared from the testes of each bird and an aliquot deriving from 10 mg of testicular tissue was used for binding assay. Specific binding of labeled LH or FSH was expressed as percentage of total radioactive hormone. Results showed significant (P < 0.05) age-related decreases in both FSH and LH receptor numbers. The highest FSH binding was found in young and middle-aged active males, with low binding in old inactive males. Testicular LH binding decreased during aging, with a sharp decrease in middle-aged males, which was similar to old males. Testosterone implants weakly stimulated FSH and LH binding in old males. Both LH and FSH binding decreased in photoregressed young males. However, testosterone implants stimulated increased LH binding, but did not affect FSH binding in young photoregressed males. These results provide evidence for separate regulation of testicular LH and FSH receptors, with testosterone stimulation of LH receptor, but not FSH receptor number in young males. However, during aging there appears to be a loss of this response, potentially because of the reduced efficacy of testosterone stimulation, thereby implying a diminished capacity for response with aging.

Impact of vinclozolin on reproductive behavior and endocrinology in Japanese quail (Coturnix coturnix japonica).

The impact of endocrine-disrupting chemicals (EDCs) has been demonstrated in mammalian models, but less research is available for avian species. The effects of vinclozolin (VIN), an antiandrogenic fungicide, on sexual differentiation and maturation were investigated in Japanese quail (Coturnix coturnix japonica). On day 4 of incubation, embryos were exposed to no treatment, oil, or 25, 50, or 100 ppm of VIN. Endpoints measured included adult male reproductive behavior, hypothalamic gonadotropin-releasing hormone I (GnRH-I) content in hatchlings and adults, plasma steroid levels in hatchlings and adults, proctodeal gland growth during maturation, and relative testicular weight at seven weeks of age. Results showed that exposure to VIN significantly (p < 0.05) altered GnRH-I in male hatchlings, whereas GnRH-I levels in females remained unaffected. Although steroid levels were unaltered by any VIN treatment, the display of male reproductive behavior seemed delayed, with the number of mounts and the number of cloacal contacts being significantly (p < 0.05) lower in the VIN-treated males. This could have an extreme negative impact on wild avian species that are routinely exposed to similar EDCs.

Exceptional cellular resistance to oxidative damage in long-lived birds requires active gene expression.

Previous studies indicated that renal tubular epithelial cells from some long-lived avian species exhibit robust and/or unique protective mechanisms against oxidative stress relative to murine cells. Here we extend these studies to investigate the response of primary embryonic fibroblast-like cells to oxidative challenge in long- and short-lived avian species (budgerigar, Melopsittacus undulatus, longevity up to 20 years, vs Japanese quail, Coturnix coturnix japonica, longevity up to 5 years) and short- and long-lived mammalian species (house mouse, Mus musculus, longevity up to 4 years vs humans, Homo sapiens, longevity up to 122 years). Under the conditions of our assay, the oxidative-damage resistance phenotype appears to be associated with exceptional longevity in avian species, but not in mammals. Furthermore, the extreme oxidative damage resistance phenotype observed in a long-lived bird requires active gene transcription and translation, suggesting that specific gene products may have evolved in long-lived birds to facilitate resistance to oxidative stress.