Effects of bisphenol-A on male reproductive success in adult Kadaknath chicken.

Bisphenol-A (BPA) adversely affects human and animal reproductive success in many ways, but this information is scant on birds. In the present study, we investigated the reproductive toxicity of BPA in adult Kadaknath chicken using two BPA dosages orally (1 or 5 mg/kg body weight) for seven weeks. In order to assess BPA toxicity, sperm functions, fertilizing ability, serum testosterone concentration and testis histopathology were measured in treated and control chickens. The semen volume was highest in birds exposed to 1mg/kg body weight BPA compared to other groups. 5 mg/kg body weight BPA reduced sperm concentration significantly more than other treatment and controls. However, overall fertility and testis histology were unaffected. These results indicate that BPA adversely affects sperm characteristics in adult kadaknath chicken without affecting fertilization potential.

Bisphenol A reduces fertilizing ability and motility by compromising mitochondrial function of sperm.

Bisphenol A (BPA) acts as an endocrine disruptor, affects animal reproductive success in vivo and affects sperm functions in vitro at environmentally relevant concentrations, leading to reduction in sperm motility and fertilizing ability in fish. The effect of in vitro BPA on avian sperm functions has not been explored. The present study examined the effect of environmentally relevant concentrations of BPA (0 mM, 0.18 mM, 0.37 mM, and 0.74 mM) on sperm functions in chicken in vitro. Sperm were exposed to concentrations of BPA for 30 min and analyzed for motility, fertilizing ability, live sperm percentage, and mitochondrial membrane potential (Δψm). Results showed that BPA at a concentration of 0.74 mM significantly decreased motility, fertilizing ability, live sperm count percentage, and sperm Δψm. Sperm motility was positively correlated with fertility (r = 0.73, p ≤ 0.01), live sperm percentage (r = 0.64, p ≤ 0.01), and high Δψm (r = 0.44, p ≤ 0.01). A dose-dependent and time-dependent effect of BPA was observed on sperm motility at all BPA concentrations. However, sperm's fertilizing ability was unaffected in low BPA concentration (0.18 mM and 0.37 mM). A significantly higher percentage of moribund sperm was observed at 0.37 mM and 0.74 mM BPA compared with at 0.18 mM BPA, in the negative control, and in the vehicle control. The present study confirms that environmentally relevant concentrations of BPA are capable of compromising sperm functions, leading to reduction in fertilizing ability of chicken sperm.

Norfloxacin drug induces reproductive toxicity and alters androgen receptor gene expression in testes and cloacal gland of male Japanese quail (Coturnix Japonica).

In an attempt to investigate the reproductive toxicity of norfloxacin in Japanese quail, male quail were given norfloxacin at 20 mg/kg body weight for 14 d. Then reproductive function and androgen receptor (AR) gene expression was examined in treated and control birds. The results of the present study indicate that fertility, cloacal gland area, sperm concentration, and serum testosterone were reduced significantly (p < 0.05) on day 14 in the norfloxacin-treated birds. Upregulation (p < 0.05) of AR mRNA was also seen in the testes on the 14th d of treatment. A trend toward downregulation of AR mRNA was seen in the cloacal gland of norfloxacin-treated birds. Histological observations revealed that norfloxacin induces cellular atrophy in testes and changes in glandular tissue in the cloacal gland. The results of the present study demonstrate that norfloxacin induces testicular toxicity in Japanese quail.

Role of nitric oxide and carbon monoxide in N(omega)-Nitro-L-arginine methyl ester-resistant acetylcholine-induced relaxation in chicken carotid artery.

The current study examined the hypothesis that acetylcholine-induced N(omega)-Nitro-L-arginine methyl ester (L-NAME)-resistant endothelium-dependent relaxations in the chicken carotid artery are mediated by nitric oxide and carbon monoxide. Acetylcholine (1 nM-3 microM) caused a concentration-dependent relaxation (pD(2) 6.81+/-0.05, R(max) 115+/-3%) of the artery segments precontracted with phenylephrine (3 microM). L-NAME (1 mM) decreased the sensitivity (pD(2) 6.44+/-0.06), but not the efficacy (R(max) 108+/-3%) of acetylcholine. It also partially decreased the acetylcholine (3 microM)-stimulated nitrite release. While treatment with N(omega)-Nitro-L-arginine (l-NNA; 1 mM) plus L-NAME (1 mM) decreased the acetylcholine-stimulated nitrite release to the basal level, it moderately inhibited (R(max) 77+/-3%) the maximal relaxation elicited with the muscarinic agonist. 2-Phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl 3-oxide (PTIO; 100 microM) a specific scavenger of nitric oxide (NO) plus the two NOS inhibitors further decreased the acetylcholine-evoked relaxation (R(max) 34+/-2%). Although soluble guanylyl cyclase (sGC) inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; 10 microM) markedly inhibited the acetylcholine-stimulated increase in tissue cGMP to less than the basal levels, it only decreased the sensitivity, but not the efficacy of the agonist either in the presence or absence of L-NAME (1 mM). Zinc Protoporphyrin-IX (ZnPP; 10 microM), a hemeoxygenase (HO) inhibitor, partially inhibited (R(max) 72+/-3%) the L-NAME-resistant acetylcholine-induced relaxations. A combined treatment of the arterial rings with L-NAME, l-NNA, PTIO and ZnPP nearly abolished (R(max) 7+/-0.9%) the vasodilator responses to acetylcholine. Endothelium removal abolished the relaxation response to acetylcholine. In conclusion, it is suggested that the acetylcholine-induced L-NAME-resistant relaxation is primarily, mediated by NO with a small but significant contribution from endothelium-derived carbon monoxide in the chicken carotid artery.