Artificial light at night (ALAN) is a major driver of firefly population declines, but its physiological effects are not well understood. To investigate the impact of ALAN on firefly development, we exposed larval Aquatica ficta fireflies to ALAN for two weeks. High larval mortality was observed in the periods of 1–68 days and 106–134 days post-treatment, which may represent the short- and long-term impacts of ALAN. We then profiled the transcriptome of larval Aquatica ficta fireflies following two weeks of ALAN exposure. A total of 1262 (1.67% out of 75777 unigenes) were differentially expressed in the treatment group: 1157 were down-regulated, and 105 were up-regulated. Up-regulated unigenes were related to regulation of hormone levels, ecdysteroid metabolic process, and response to stimulus; down-regulated unigenes were related to negative regulation of insulin receptor signaling, germ cell development, oogenesis, spermatid development, and regulation of neuron differentiation. Transcriptome results suggest that the endocrine, reproductive, and neural development of firefly larvae could be impaired by even relatively brief period of ALAN exposure. This report contributes a much-needed molecular perspective to the growing body of research documenting the fitness impacts of ALAN on bioluminescent fireflies.

Microplastics (<5 mm) are ubiquitous in the global environment and are increasingly recognized as a biological hazard, particularly in the oceans. Zooplankton, at the base of the marine food web, have been known to consume microplastics. However, we know little about the impacts of microplastics across life history stages and on carbon settling. Here, we investigated the effects of ingestion of neutrally buoyant polystyrene beads (6.68 μm) by the copepod Acartia tonsa on (1) growth and survival across life history stages, (2) fecundity and egg quality, (3) and fecal characteristics. We found that microplastic exposure reduced body length and survival for nauplii and resulted in smaller eggs when copepods were exposed during oogenesis. Combining these life history impacts, our models estimate a 15% decrease in population growth leading to a projected 30-fold decrease in abundance over 1 year or 20 generations with microplastic exposure. In addition, microplastic-contaminated fecal pellets were 2.29-fold smaller and sinking rates were calculated to be 1.76-fold slower, resulting in an estimated 4.03-fold reduction in fecal volume settling to the benthos per day. Taken together, declines in population sizes and fecal sinking rates suggest that microplastic consumption by zooplankton could have cascading ecosystem impacts via reduced trophic energy transfer and slower carbon settling.

Dibutyl phthalate (DBP), one of the most widely used plasticizers, is a known environmental endocrine disruptor that impairs male and female fertility. In this study, oral administration of DBP was given to pregnant mice on 14.5 days post coitus (dpc) for 3 days; and additionally, DBP was added into the culture of 14.5 dpc fetal ovaries for 3 days. DBP exposure during gestation disturbed the progression of meiotic prophase I of mouse oocytes, specifically from the zygotene to pachytene stages. Meanwhile, the DBP-exposed pachytene oocytes showed increased homologous recombination sites and unrepaired DNA damage. Furthermore, DBP caused DNA damage by increasing oxidative stress, decreased the expression of multiple critical meiotic regulators, and consequently induced oocyte apoptosis. Moreover, the effect of DBP on meiosis I prophase involved estrogen receptors α and β. Collectively, these results demonstrated a set of meiotic defects in DBP-exposed fetal oocytes. As aberrations in homologous recombination can result in aneuploid gametes and embryos, this study provides new support for the deleterious effects of phthalates.

It is known that Di (2-ethylhexyl) phthalate (DEHP) may impact mammalian reproduction and that in females one target of the drug’s action is follicle assembly. Here we revisited the phthalate’s action on the ovary and from bioinformatics analyses of the transcriptome performed on newborn mouse ovaries exposed in vitro to DEHP, up-regulation of PDE3A, as one of the most important alterations caused by DEHP on early folliculogenesis, was identified. We obtained some evidence suggesting that the decrease of cAMP level in oocytes and the parallel decrease of PKA expression, consequent on the PDE3A increase, were a major cause of the reduction of follicle assembly in the DEHP-exposed ovaries. In fact, Pde3a RNAi on cultured ovaries reducing cAMP and PKA decrease counteracted the primordial follicle assembly impairment caused by the compound. Moreover, RNAi normalized the level of Kit, Nobox, Figla mRNA and GDF9, BMP15, CX37, γH2AX proteins in oocytes, and KitL transcripts in granulosa cells as well as their proliferation rate altered by DEHP exposure. Taken together, these results identify PDE3A as a new critical target of the deleterious effects of DEHP on early oogenesis in mammals and highlight cAMP-dependent pathways as major regulators of oocyte and granulosa cell activities crucial for follicle assembly. Moreover, we suggest that the level of intracellular cAMP in the oocytes may be an important determinant for their capability to repair DNA lesions caused by DNA damaging compounds including DEHP.

Ciprofloxacin (CFX) and ofloxacin (OFX) are two of the most often used fluoroquinolone antibiotics, and their residues are found in large amounts in various aquatic settings. However, the toxicity tests of CFX using eukaryotic organisms such as Daphnia magna are inadequate, and the test result of OFX is currently unknown. Therefore, the chronic toxicity test for D. magna was performed during 42 days under exposure to CFX and OFX concentrations of 50, 500, and 5000 μg L⁻¹. All exposure conditions did not cause mortality for D. magna. CFX exposure at 500 μg L⁻¹ resulted in an earlier oogenesis date and increased brood size in the second birth. The Poisson-based generalized linear mixed-effects model revealed that the reduction of fertility was statistically significant for the CFX and OFX exposures at 5000 μg L⁻¹. On the other hand, the production of dead eggs as offspring degradation was also found significantly as maternal D. magna exposed to antibiotics at 5000 μg L⁻¹. In addition, following long-term exposure to antibiotics, maternal adaptation to antibiotics was established for offspring deterioration and fertility. However, the OFX exposure showed that the fertility-suppressed effects continued for a longer period than the CFX exposure. Although no rational explanation has yet been given for the more substantial effect of OFX on reducing fertility than CFX, molecular cell biology and symbiotic microbial flora derived from previous studies could explain our ecotoxicological results. This study is the first report for the OFX chronic toxicities on D. magna by comparing it to the toxicity of CFX. Our study contributes to guiding the future impact assessment of fluoroquinolone antibiotic pollution on ecosystems, including the need for new statistical methods in ecotoxicological studies.

Bisphenol S (BPS) is an endocrine disruptor which is widely used in commercial plastic products. Previous studies have shown that exposure to BPS has toxic effects on various aspects of mammalian, but there are few reports about reproductive toxicity. In order to investigate the effects of maternal BPS exposure on the reproductive of F1 and F2 female mice, the pregnant mice were orally administered with different dosages of BPS only once every day from 12.5 to 15.5 days post-coitus (dpc). The results showed that maternal BPS exposure to 2 μg per kg of body weight per day (2 μg/kg) and 10 μg/kg accelerated the meiotic prophase I (MPI) of F1 female mice and the expression of the genes related to meiotic were increased. Further studies showed that maternal BPS exposure resulted in a significant increase in the percentage of oocytes enclosed in primordial follicles in the 3 days post-partum (3 dpp) ovaries of F1 female mice. And at the time of 21 days post-partum (21 dpp) in F1 female mice, the number of antral follicles were significantly lower compare to controls. In the study of five-week female mice of F1, we found that BPS disturbed the folliculogenesis, and the maturation rates and fertilization rates of oocytes were significantly decreased. Of note, maternal BPS exposure disrupted H3K4 and H3K9 tri-methylation levels in F1 ovaries. Maternal BPS exposure only affected the cyst breakdown in F2 female mice. Taken together, our results suggest that, maternal BPS exposure impaired the process of meiosis and oogenesis of F1 and F2 offspring, resulting in abnormal follicular development and serious damage to the reproduction.

HT-2 toxin (HT-2), a mycotoxin produced by Fusarium species, is detected in a variety of cereal grain-based human food and animal feed. Apart from its well-established immunotoxicity and haematotoxicity, it also causes reproductive disorders. In the present study, we revealed the adverse effects of HT-2 on early oogenesis at the foetal stage. Pregnant mice were orally administered with HT-2 for 3 days at mid-gestation. Oocytes from female foetuses exposed to HT-2 displayed defects in meiotic prophase, including unrepaired DNA damage, elevated recombination levels, and reduced expression of meiotic-related genes. Subsequently, increased oxidative stress was observed in the foetal ovaries exposed to HT-2, along with the elevated levels of reactive oxygen species, malondialdehyde, catalase, and superoxide dismutase 1/2, thereby resulting in impaired mitochondrial membrane potential and cell apoptosis. Furthermore, pre-treatment with urolithin A, a natural compound with antioxidant activities, partially reversed the delayed meiotic process by alleviating oxidative stress. Since early oogenesis is essential to determine female fertility in adult life, this study indicated that brief maternal exposure to HT-2 toxin may compromise the fertility of a developing female foetus.

Microplastic transfer between horseshoe crabs (Limulus polyphemus) and migratory shorebirds through consumption of crab eggs was examined in Jamaica Bay, New York. Fertilized and unfertilized crab eggs, shorebird fecal pellets, beach sand, and bay water were processed with a hydrogen peroxide solution to remove organic material, then stained with a Nile Red to identify microplastics using fluorescence microscopy. Microplastics were present in all samples and ranged from approximately26–1300 μm. Unfertilized and fertilized eggs contained significantly higher numbers of microplastic particles per gram than shorebird fecal pellets, beach sand, and bay water. The presence of microplastics in unfertilized egg samples indicates that microplastics undergo maternal transfer during oogenesis. We estimated that 1 g of horseshoe crab eggs could contain approximately 426 to 840 microplastic particles, suggesting that shorebirds feeding on this resource could be ingesting a substantial burden of microplastics during their migratory stopover, much of which appears to be retained by shorebirds, rather than being eliminated in their fecal pellets.

Early embryonic arrest (EEA) leads to cancelation of fresh cycles among infertile women undergoing in vitro fertilization (IVF), bringing a great challenge for IVF. Whether exposure to thallium (Tl) is associated with an increased risk of EEA, especially its interaction with polymorphisms of mitochondria DNA (mtDNA) gene, is worthy of study. A case–control design was performed, including 74 EEA cases with 123 IVF cycles and 157 age and BMI-matched controls with 180 IVF cycles. Levels of Tl and other toxic metals (lead (Pb), (mercury) Hg, and (arsenci) As) were assessed by measuring them in blood samples collected on the day of oocyte retrieval; PCR amplification and sequencing were performed to screen the polymorphic sites of mtDNA gene in D-loop region. Bayesian kernel machine regression (BKMR) was used to confirm that Tl played a leading role in the situation of combined exposure; generalized estimating equation (GEE) models were used to evaluate the associations of Tl concentrations, polymorphisms of mtDNA gene, and their interactions with the risk of EEA. The impact of Tl exposure or polymorphisms of mtDNA gene on the oogenesis and embryonic development was also evaluated. BKMR analysis revealed that PIP (posterior inclusion probability) value of T1 was 0.9096, indicating that it played a leading role in the situation of combined exposure. Compared to the first quartile of Tl, the adjusted ORs (95% CIs) of EEA risk were 0.66 (0.26, 1.70), 1.18 (0.52, 2.64), and 4.53 (2.11, 9.69) for the second, third, and fourth quartile, respectively (p trend < 0.001). Compared to the wild type of mtDNA 16,519 gene (T 16,519 T), the adjusted OR (95% CI) of EEA risk for the variant type (T 16,519 C) was 3.11 (1.70, 5.72), and the variant types of the other sites with a minor allele frequency > 10% were not significantly related with the risk of EEA after FDR (False Discovery Rate) correction. With respect to interaction, compared to women at low Tl exposure level & wild type of mtDNA 16,519 gene group, the adjusted OR (95% CI) of EEA risk for women at high Tl exposure level & variant type of mtDNA 16,519 gene group was 9.28 (3.33, 25.81). Additionally, Tl exposure and polymorphisms of mtDNA 16,519 gene are inversely associated with the outcomes of oogenesis and embryonic development significantly. Our study indicated that high Tl exposure level was associated with the increased risk of EEA and Tl played a leading role in the situation of combined exposure; the strength of association was much higher when Tl exposure interacted with polymorphism of 16,519 mtDNA gene. These relationships might originate from the impact of Tl exposure or polymorphism of 16,519 mtDNA gene on the oogenesis and early embryonic development in vitro. Infertile women should keep high vigilant against Tl exposure especially those with variant type of mtDNA 16,519 gene.