Imazapyr herbicideformulation induced multiple abnormalities in gonadal development of Xenopus laevis at environmentally relevant concentrations

Mankind is now in the era of environmental contamination and pollution, where the environment has become a warehouse of its several toxicants. In fact, there are no longer any pristine area without these anthropogenic toxicants, with serious consequences on wildlife’s physiological processes including growth and reproduction. The widespread occurrence of pesticides for example, is being linked to numerous reproductive malformations in wildlife organisms, but the degree of association has not been characterised. Using the extended Xenopus Metamorphosis Assay (XEMA) protocol, the exposure impacts of imazapyr herbicide formulation (Arsenal), approved for aquatic environment was assessed on gonadal development of Xenopus laevis at environmentally relevant concentrations of 0.5, 2.0, and 3.5 mg/L. The formulation significantly reduced the mean body mass at premetamorphosis (NF-stage 55) at 3.5 mg/L concentration compared to the control. In sex ratio, the exposure only showed marginal fluctuations at all the exposure concentrations. For gonadal malformations, an abnormality index of 17.5%, 25%, and 35% was derived at 0.5 mg/L, 2.0, and 3.5 mg/L concentrations respectively, with malformations including tissues separation, segmented aplasia, aplasia, mixed sex, narrow hypoplasia, and angular deformity. This study showed that at relevant environmental concentrations, this formulation induced concentration dependent complex gonadal malformations, suggesting its potential capacities to induced serious reproductive disruptions that can negatively impacts fecundity, fertility, and general reproductive fitness of amphibians. In order to protect the wildlife from reproductive impacts, there is a serious need for cautions in application of this herbicide formulation

Extensive reproductive disruption, ovarian masculinization and aromatase suppression in Atlantic croaker in the northern Gulf of Mexico hypoxic zone

The long-term impacts on marine ecosystems of the recent dramatic worldwide increase in the incidence of coastal hypoxia are unknown. Here, we show widespread reproductive disruption in Atlantic croakers collected from hypoxic sites approximately 120 km apart in the extensive northern Gulf of Mexico continental shelf hypoxic zone. Gonadal growth and gamete production were impaired in croakers from hypoxic sites compared with fish from reference normoxic sites east of the Mississippi River Delta. Male germ cells were detected in approximately 19 per cent of croaker ovaries collected in the hypoxic region, but were absent in ovaries from normoxic sites. In addition, the sex ratio was skewed towards males at the hypoxic sites. The masculinization and other reproductive disruptions were associated with declines in neuroendocrine function, as well as ovarian and brain expression of aromatase (the enzyme that converts androgens to oestrogens). A similar incidence of ovarian masculinization and decline in ovarian aromatase expression were observed in croaker after chronic laboratory hypoxia exposure, indicating that ovarian masculinization is a specific hypoxia response and is due to decreased aromatase activity. The results suggest severe reproductive impairment can occur over large coastal regions in marine fish populations exposed to seasonal hypoxia, with potential long-term impacts on population abundance.

Developmental Programming: Excess Weight Gain Amplifies the Effects of Prenatal Testosterone Excess On Reproductive Cyclicity—Implication for Polycystic Ovary Syndrome

Sheep exposed to testosterone (T) during early to midgestation exhibit reproductive defects that include hypergonadotropism, functional hyperandrogenism, polycystic ovaries, and anovulatory infertility, perturbations similar to those observed in women with polycystic ovary syndrome. Obesity increases the severity of the phenotype in women with polycystic ovary syndrome. To determine whether prepubertal weight gain would exaggerate the reproductive disruptions in prenatal T-treated sheep, pregnant sheep were injected with 100 mg T propionate (∼1.2 mg/kg) im twice weekly, from d 30–90 of gestation. Beginning about 14 wk after birth, a subset of control and prenatal T-treated females were overfed to increase body weight to 25% above that of controls. Twice-weekly progesterone measurements found no differences in timing of puberty, but overfed prenatal T-treated females stopped cycling earlier. Detailed characterization of periovulatory hormonal dynamics after estrous synchronization with prostaglandin F2α found 100% of controls, 71% of overfed controls, 43% of prenatal T-treated, and 14% of overfed prenatal T-treated females had definable LH surges. Only one of seven overfed prenatal T-treated female vs. 100% of control, 100% of overfed control, and seven of eight prenatal T-treated females exhibited a luteal progesterone increase. Assessment of LH pulse characteristics during the anestrous season found both overfeeding and prenatal T excess increased LH pulse frequency without an interaction between these two variables. These findings agree with the increased prevalence of anovulation observed in obese women with polycystic ovary syndrome and indicate that excess postnatal weight gain amplifies reproductive disruptions caused by prenatal T excess. Exposure of sheep to excess testosterone in utero disrupts reproductive cyclicity, with postpubertal excess weight gain amplifying the severity of this adult reproductive phenotype.