Rational Design of Conjugated Acetylenic Polymers Enables a Two-Electron Water Oxidation Pathway for Enhanced Photosynthetic Hydrogen Peroxide Generation.

Herein, the design of conjugated acetylenic polymers (CAPs) featuring diverse spatial arrangements and intramolecular spacers of diacetylene moieties (─C≡C─C≡C─) for photocatalytic hydrogen peroxide (H2 O2 ) production from water and O2 , without the need for sacrificial agents, is presented. It is shown that the linear configuration of diacetylene moieties within conjugated acetylenic polymers (CAPs) induces a pronounced polarization of electron distribution, which imparts enhanced charge-carrier mobility when compared to CAPs' networks featuring cross-linked arrangements. Moreover, optimizing the intramolecular spacer between diacetylene moieties within the linear structure leads to the exceptional modulation of the band structures, specifically resulting in a downshifted valence band (VB) and rendering the two-electron water oxidation pathway thermodynamically feasible for H2 O2 production. Consequently, the optimized CAPs with a linear configuration (LCAP-2), featuring spatially separated reduction centers (benzene rings) and oxidation centers (diacetylene moieties), exhibit a remarkable H2 O2 yield rate of 920.1 µmol g-1 h-1 , superior than that of the linear LCAP-1 (593.2 µmol g-1 h-1 ) and the cross-linked CCAP (433.4 µmol g-1 h-1 ). The apparent quantum efficiency (AQE) and solar-to-chemical energy conversion (SCC) efficiency of LCAP-2 are calculated to be 9.1% (λ = 420 nm) and 0.59%, respectively, surpassing the performance of most previously reported conjugated polymers.

Unraveling the Fundamentals of Axial Coordination FeN4+1 Sites Regulating the Peroxymonosulfate Activation for Fenton-Like Activity.

Precise modulation of the axial coordination microenvironment in single-atom catalysts (SACs) to enhance peroxymonosulfate (PMS) activation represents a promising yet underexplored approach. This study introduces a pyrolysis-free strategy to fabricate SACs with well-defined axial-FeN4+1 coordination structures. By incorporating additional out-of-plane axial nitrogen into well-defined FeN4 active sites within a planar, fully conjugated polyphthalocyanine framework, FeN4+1 configurations are developed that significantly enhance PMS activation. The axial-FeN4+1 catalyst excelled in activating PMS, with a high bisphenol A (BPA) degradation rate of 2.256 min-1, surpassing planar-FeN4/PMS systems by 6.8 times. Theoretical calculations revealed that the axial coordination between N and the Fe sites forms an optimized axial FeN4+1 structure, disrupting the electron distribution symmetry of Fe and optimizing the electron distribution of the Fe 3d orbital (increasing the d-band center from -1.231 to -0.432 eV). Consequently, this led to an enhanced perpendicular adsorption energy of PMS from -1.79 to -1.82 eV and reduced energy barriers for the formation of the key reaction intermediate (O*) that generates 1O2. This study provides new insights into PMS activation through the axial coordinated engineering of well-defined SACs in water purification processes.

Induction of sperm hypermotility through membrane progestin receptor alpha (mPRα): A teleost model of rapid, multifaceted, nongenomic progestin signaling.

Rapid progestin effects on sperm physiology have been described in a variety of vertebrate species. Here, we briefly review the signaling pathways mediating rapid progestin induction of sperm hypermotility and increased fertility in two teleost species, Atlantic croaker and southern flounder. Acute in vitro treatment of teleost sperm with the progestin hormone, 20ß-S, causes activation of progestin membrane receptor alpha (mPRα, or Paqr7) coupled to a stimulatory olfactory G protein (Golf), resulting in increased cAMP and calcium concentrations and hypermotility upon activation in a hyperosmotic medium. Pharmacological tools were used to investigate the involvement of mPRα and several intracellular signaling pathways in the hypermotility response. Evidence was obtained using the specific mPRα agonist, Org OD 02-0, that this progestin action is mediated through mPRα and not through the nuclear PR. The results indicate that progestins induce hypermotility through activation of a membrane adenylyl cyclase (Acy)/cAMP pathway, an epidermal growth factor receptor (Egfr)/Mapkinase pathway, and a Pi3kinase/Akt/phosphodiesterase (Pde) pathway which result in increased sperm calcium concentrations within 10 s. The finding that inhibition of any one of these pathways is sufficient to prevent hypermotility along with the calcium increase suggests that activation of all of them and the associated calcium increase are required for the progestin hypermotility response. On the basis of these findings a model of progestin induction of sperm hypermotility in teleosts is proposed. As teleosts lack CatSper, the model described here is a non-CatSper mediated one and may therefore be applicable to a wide variety of nonmammalian vertebrates.

Activation of the Pi3k/Akt pathway and modulation of phosphodiesterase activity via membrane progestin receptor-alpha (mPRalpha) regulate progestin-initiated sperm hypermotility in Atlantic croaker.

Rapid progestin stimulation of sperm motility is a widely observed phenomenon in vertebrates, but the mechanisms governing these effects are still poorly understood, especially in teleosts, amphibians, and birds, which do not express CatSper. Here we show that progestin-stimulated sperm hypermotility in a teleost, Atlantic croaker (Micropogonias undulatus), is initiated though membrane progestin receptor-alpha (mPRalpha, also known as Paqr7b) and involves activation of the Pi3k/Akt pathway and increased phosphodiesterase (Pde) activity. The specific mPRalpha agonist 10-ethenyl-19-norprogesterone (Org OD 02-0) mimicked the stimulatory actions of the endogenous progestin in this species, 17, 20beta, 21-trihydroxy-4-pregnen-3-one (20beta-S), on sperm motility. Inhibition of Pi3k (1 nM Wortmannin; 25 µM LY294002) and Akt (25 µM ML-9) effectively abolished progestin-initiated sperm hypermotility. Surprisingly, treatment with the PDE inhibitors Cilostamide (100 nM) and Rolipram (1 µM) also blocked progestin stimulation of sperm motility. Whereas treatment with 20beta-S increased sperm Pde activity, pretreatment with Wortmannin eliminated this response to the progestin and also resulted in elevated cAMP levels, indicating that Pdes are at least partially under Pi3k/Akt control. The results suggest that mPRalpha-mediated progestin stimulation of sperm motility in croaker through Pi3k/Akt is dependent on maintenance of Pde activity and a reduction in internal cAMP concentrations. However, a previous study showed that progestin stimulation of sperm hypermotility in this species is also dependent on membrane adenylyl cyclase (Acy) activation and increased intrasperm cAMP concentrations. Collectively, these findings indicate that progestin-mediated hypermotility through mPRalpha in teleost sperm involves modulation of intracellular cAMP concentrations through multiple signaling pathways.

Membrane progestin receptor alpha mediates progestin-induced sperm hypermotility and increased fertilization success in southern flounder (Paralichthys lethostigma).

Progestin hormones stimulate sperm motility in teleosts but their mechanisms of action remain unclear. Preliminary results suggest that progestin upregulation of sperm motility in southern flounder and several other marine species is mediated through a sperm membrane progestin receptor with the characteristics of membrane progestin receptor alpha (mPRα, also known as Paqr7b). The hypothesis that mPRα has an important role in progestin regulation of southern flounder sperm motility and fertility was tested in the present study. The specific mPRα agonist, 10-ethenyl-19-norprogesterone (Org OD 02-0, 100nM), mimicked the stimulatory actions of the endogenous progestin, 17,20ß, 21-trihydroxy-4-pregnen-3-one (20ß-S, 100nM) on flounder sperm motility. The concentration of the mPRα protein on sperm plasma membranes was positively correlated to sperm motility as well as the responsiveness of sperm to progestin stimulation. Acute in vitro progestin treatment of sperm with high mPRα protein levels increased both sperm motility and fertilization success in strip spawning experiments. However, in vitro progestin treatments were ineffective on sperm with low receptor abundance. A single injection of the superactive gonadotropin-releasing hormone analog (LHRHa, 100µg/kg) increased sperm motility and fertilization success in strip spawning experiments 72h post-injection which was accompanied by an increase in mPRα protein concentrations on sperm plasma membranes. These results provide clear evidence that southern flounder sperm hypermotility is mediated through mPRα. Stimulatory G proteins, but not inhibitory G proteins, were identified in flounder sperm plasma membrane fractions. The finding that treatment of flounder sperm plasma membrane fractions with either 20ß-S or Org OD 02-0 increases cAMP levels suggests progestins stimulate flounder sperm motility by activating an mPRα/stimulatory G protein/membrane adenylyl cyclase pathway. A similar mechanism has been identified in Atlantic croaker, suggesting that the signaling pathway mediated by mPRα in sperm is highly conserved in advanced teleosts. Collectively, our results indicate that progestin-stimulation of flounder sperm hypermotility and fertility is dependent on a sufficient concentration of mPRα which can be upregulated by in vivo LHRHa treatments. These findings potentially have practical applications for enhancing the fertility of male flounder broodstock.

Identification of 17,20ß,21-trihydroxy-4-pregnen-3-one (20ß-S) receptor binding and membrane progestin receptor alpha on southern flounder sperm (Paralichthys lethostigma) and their likely role in 20ß-S stimulation of sperm hypermotility.

The existence of direct progestin actions on teleost sperm to stimulate hypermotility is not widely acknowledged because it has only been demonstrated in members of the family Sciaenidae. In the present study, progestin stimulation of sperm hypermotility was investigated in a non-sciaenid, southern flounder, and the potential role of membrane progestin receptor alpha (mPRα or Paqr7b) in mediating this action was examined. The major progestin produced in vitro by flounder testicular fragments co-migrated with 17,20ß,21-trihydroxy-4-pregnen-3-one (20ß-S) during thin-layer chromatography. Treatment of flounder sperm with 5 nM-100 nM 20ß-S significantly increased sperm velocity in vitro, whereas 17,20ß-dihydroxy-4-pregnen-3-one and other steroids were ineffective. A single class of high affinity (K(d) 22.95 nM), saturable, limited-capacity binding sites (B(max) 0.013 nM) specific for 20ß-S was identified on sperm membranes. Treatment of sperm membranes with guanosine 5'-(3-O-thio)triphosphate reduced [(3)H]-20ß-S binding, suggesting the 20ß-S receptor couples to a G protein. The membrane adenylyl cyclase inhibitor 2',5'-dideoxyadenosine blocked 20ß-S-induced sperm hypermotility, indicating 20ß-S activates stimulatory G proteins. Finally, flounder paqr7b was cloned and characterized from testicular tissues. The Paqr7b protein is expressed on the midpiece of flounder sperm and is more abundant in individuals with high sperm motility than low motility donors. These findings suggest that 20ß-S stimulates sperm hypermotility in flounder through activation of stimulatory G proteins, likely through Paqr7b. The finding that progestins directly stimulate sperm hypermotility in a flatfish, a highly derived species not belonging to the teleost family Sciaenidae, suggests this phenomenon is widespread among advanced fishes.

Involvement of epidermal growth factor receptors and mitogen-activated protein kinase in progestin-induction of sperm hypermotility in Atlantic croaker through membrane progestin receptor-alpha.

The intracellular pathways mediating rapid, nongenomic progestin stimulation of sperm motility remain unclear. The role of epidermal growth factor receptors (Egfr and ErbB2) and mitogen-activated protein kinase (Mapk) in membrane progestin receptor-alpha (mPRα)-mediated progestin stimulation of sperm hypermotility was examined in a teleost, Atlantic croaker. Inhibition of upstream regulators of Egfr, intracellular tyrosine kinase (Src) with PP2, and matrix metalloproteinase (MMP) with Ilomastat, abolished progestin-initiated sperm hypermotility by 17,20ß,21-trihydroxy-4-pregnen-3-one (20ß-S; 20 nM) and a specific mPRα agonist, Org OD 02-0 (20 nM). Pretreatment of croaker sperm with EGFR inhibitors, AG1478 (5 µM) and RG13022 (50 µM), the ErbB2 inhibitor, AG879 (5 nM), or the MEK1/2 inhibitor, U0126 (500 nM) blocked progestin stimulation of sperm motility. Levels of phosphorylated extracellular-related kinase 1 and 2 (P-Erk1/2) were increased after 20ß-S treatment. These results demonstrate that progestin-mediated hypermotility via mPRα in croaker sperm involves activation of the Egfr, ErbB2 and Mapk pathways.

Impaired gamete production and viability in Atlantic croaker collected throughout the 20,000 km(2) hypoxic region in the northern Gulf of Mexico.

The long-term impacts of recent marked increases in the incidence and extent of hypoxia (dissolved oxygen <2 mg/L) in coastal regions worldwide on fisheries and ecosystems are unknown. Reproductive impairment was investigated in Atlantic croaker collected in 2010 from the extensive coastal hypoxic region in the northern Gulf of Mexico. Potential fecundity was significantly lower in croaker collected throughout the ~20,000 km(2) hypoxic region than in croaker from normoxic sites. In vitro bioassays of gamete viability showed reductions in oocyte maturation and sperm motility in croaker collected from the hypoxic sites in response to reproductive hormones which were accompanied by decreases in gonadal levels of membrane progestin receptor alpha, the receptor regulating these processes. The finding that environmental hypoxia exposure reduces oocyte viability in addition to decreasing oocyte production in croaker suggests that fecundity estimates need to be adjusted to account for the decrease in oocyte maturation.