Efficient Photoelectrochemical Water Splitting over Anodized <i>p</i>‑Type NiO Porous Films

NiO photocathodes were fabricated by alkaline etching-anodizing nickel foil in an organic-based electrolyte. The resulting films have a highly macroporous surface structure due to rapid dissolution of the oxide layer as it is formed during the anodization process. We are able to control the films’ surface structures by varying the anodization duration and voltage. With an onset potential of +0.53 V versus the reversible hydrogen electrode (RHE), the photocurrent efficiency of the NiO electrodes showed dependencies on their surface roughness factor, which determines the extent of semiconductor-electrolyte interface and the associated quality of the NiO surface sites. A maximum incident photon-to-current conversion efficiency (IPCE_max) of 22% was obtained from NiO film with a roughness factor of 8.4. Adding an Al₂O₃ blocking layer minimizes surface charge recombination on the NiO and hence increased the IPCE_max to 28%. The NiO/Al₂O₃ films were extremely stable during photoelectrochemical water splitting tests lasting up to 20 h, continuously producing hydrogen and oxygen in the stoichiometric 2:1 ratio. The NiO/Al₂O₃ and NiO films fabricated using the alkaline anodization process produced 12 and 6 times as much hydrogen, respectively, as those fabricated using commercial NiO nanoparticles

Identification of Molecular Targets for 4,5-Dichloro-2‑<i>n</i>‑octyl-4-isothiazolin-3-one (DCOIT) in Teleosts: New Insight into Mechanism of Toxicity

Environmental pollutants are capable of concomitantly inducing diverse toxic effects. However, it is largely unknown which effects are directly induced and which effects are secondary, thus calling for definitive identification of the initiating molecular event for a pollutant to elucidate the mechanism of toxicity. In the present study, affinity pull-down assays were used to identify target proteins for 4,5-dichloro-2-<i>n</i>-octyl-4-isothiazolin-3-one (DCOIT), a costal pollutant of emerging concern, in various tissues (e.g., brain, liver, plasma, and gonad) from marine medaka (<i>Oryzias melastigma</i>) and zebrafish (<i>Danio rerio</i>). Pull-down results showed that, in male and female brains from medaka and zebrafish, DCOIT had a consistently high affinity for G protein alpha subunits (Gα), suggesting the targeted effects of DCOIT on signaling transduction from G protein-coupled receptors (GPCRs) and an extrapolatable mode of action in teleost brains. Validation using recombinant proteins and molecular docking analysis confirmed that binding of DCOIT to Gα protein competitively inhibited its activation by substrate. Considering the involvement of GPCRs in the regulation of myriad biological processes, including the hypothalamus–pituitary–gonadal–liver axis, binding of DCOIT to upstream Gα proteins in the brain may provide a plausible explanation for the diversity of toxic effects resulting from DCOIT challenge, especially abnormal hormonal production through the mitogen-activated protein kinase pathway. A new mechanism of action based on GPCR signaling is thus hypothesized for endocrine disrupting chemicals and warrants further research to clearly elucidate the link between GPCR signaling and endocrine disruption

Endocrine Disruption throughout the Hypothalamus–Pituitary–Gonadal–Liver (HPGL) Axis in Marine Medaka (<i>Oryzias melastigma</i>) Chronically Exposed to the Antifouling and Chemopreventive Agent, 3,3′-Diindolylmethane (DIM)

Despite being proposed as a promising antifouling and chemopreventive agent, the environmental risks of 3,3′-diindolylmethane (DIM) are scarcely investigated. Therefore, this study used adult marine medaka (<i>Oryzias melastigma</i>) as a model organism to examine the toxicological effects and underlying mechanism of DIM throughout the hypothalamus–pituitary–gonadal–liver (HPGL) axis following 28 days of exposure to low DIM concentrations (0 and 8.46 μg/L). The results showed that altered gene transcription in the hypothalamus, pituitary, and gonads contributed to the great imbalance in hormone homeostasis. The lowered estradiol (E₂)/testosterone (T) and E₂/11-keto-testosterone (11-KT) ratios in female plasma resulted in decreased synthesis and levels of vitellogenin (VTG) and choriogenin in the liver and plasma, and vice versa in males. Subsequently, VTG and choriogenin deficiency blocked the reproductive function of the ovary as indicated by decreased fecundity and offspring viability, whereas in male medaka, DIM mainly targeted the liver and induced severe vacuolization. Proteomic profiling of plasma revealed that the sex-specific susceptibility to DIM could be attributed to the increased detoxification and oxidative defense in males. Overall, this study identified the endocrine disruption and reproductive impairment potency of DIM and first elucidated its mechanisms of action in medaka. The differential responses to DIM (estrogenic activities in the male but antiestrogenic activities in the female) provided sensitive biomarkers characteristic of each sex. Considering the chemical stability and potent endocrine disturbance at low concentration, the application of DIM either as an antifouling or chemopreventive agent should be approached with caution in marine environments

Chronic Exposure of Marine Medaka (<i>Oryzias melastigma</i>) to 4,5-Dichloro-2‑<i>n</i>‑octyl-4-isothiazolin-3-one (DCOIT) Reveals Its Mechanism of Action in Endocrine Disruption via the Hypothalamus-Pituitary-Gonadal-Liver (HPGL) Axis

In this study, marine medaka (<i>Oryzias melastigma</i>) were chronically exposed for 28 days to environmentally realistic concentrations of 4,5-dichloro-2-<i>n</i>-octyl-4-isothiazolin-3-one (DCOIT) (0, 0.76, 2.45, and 9.86 μg/L), the active ingredient in commercial antifouling agent SeaNine 211. Alterations of the hypothalamus-pituitary–gonadal-liver (HPGL) axis were investigated across diverse levels of biological organization to reveal the underlying mechanisms of its endocrine disruptive effects. Gene transcription analysis showed that DCOIT had positive regulatory effects mainly in male HPGL axis with lesser extent in females. The stimulated steroidogenic activities resulted in increased concentrations of steroid hormones, including estradiol (E₂), testosterone (T), and 11-KT-testosterone (11-KT), in the plasma of both sexes, leading to an imbalance in hormone homeostasis and increased E₂/T ratio. The relatively estrogenic intracellular environment in both sexes induced the hepatic synthesis and increased the liver and plasma content of vitellogenin (VTG) or choriogenin. Furthermore, parental exposure to DCOIT transgenerationally impaired the viability of offspring, as supported by a decrease in hatching and swimming activity. Overall, the present results elucidated the estrogenic mechanisms along HPGL axis for the endocrine disruptive effects of DCOIT. The reproductive impairments of DCOIT at environmentally realistic concentrations highlights the need for more comprehensive investigations of its potential ecological risks

Multigenerational Disruption of the Thyroid Endocrine System in Marine Medaka after a Life-Cycle Exposure to Perfluorobutanesulfonate

Accumulation of perfluorobutanesulfonate (PFBS) is frequently detected in biota, raising concerns about its ecological safety. However, hazardous effects of PFBS remain largely unexplored, especially for endocrine disrupting potency. In the present study, the multigenerational endocrine disrupting potential of PFBS was investigated by exposing F0 marine medaka eggs to PFBS at different concentrations (0, 1.0, 2.9, and 9.5 μg/L) until sexual maturity. The F1 and F2 generations were reared without continued exposure. Thyroidal disturbances were examined in all three generations. PFBS exposure decreased the levels of 3,5,3′-triiodothyronine (T3) in F0 female blood; however, it increased T3 or thyroxine (T4) levels in F0 brains, in which hyperthyroidism suppressed the local transcription of 5′-deiodinase 2 (<i>Dio2</i>). Obviously decreased T3 was transferred to F1 eggs, although the parental influences were reversed in F1 larvae. Delayed hatching was coupled with elevated T3 levels in F1 larvae. F1 adults showed comparable symptoms of thyroidal disruption with F0 adults. A slight recovery was noted in the F2 generation, although F2 larvae still exhibited thyroid disruption and synthesized excessive T4. Our results suggested that the offspring suffered more severe dysfunction of the thyroidal axis albeit without direct exposure. This study provided the first molecular insight about PFBS toxicology on the thyroid, beneficial to both human and environmental risk assessment