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Solar-driven interfacial evaporation technology stands out as a promising solution for sustainable freshwater production. To achieve sustained and efficient water evaporation, it is crucial to carefully modulate the distribution of water content within the solar evaporator. In this study, a novel light-temperature responsive composite hydrogel-based solar evaporator was successful constructed. This involved the incorporation of a hydrophilic backbone (polyacrylamide) and a highly efficient solar absorber (multi-walled carbon nanotubes) into a temperature-sensitive hydrogel polymer backbone (poly (N, N-diethylacrylamide)). Due to its low critical solution temperature, the evaporator can undergo a hydrophilic/hydrophobic phase transition alternating day and night conditions. In natural sunlight, the upper hydrogel evaporation region is rendered hydrophobic, minimizing heat loss and preventing salt crystallization. Simultaneously, the bottom water delivery region is hydrophilic to ensure sufficient water supply. At night, the evaporator absorbs water and dissolves, thereby facilitating the rapid return of highly concentrated brine. Leveraging the spontaneously formed Janus structure, the photo-hydrothermal hydrogel achieves an impressive evaporation rate of 2.74 kg m−2 h−1 and exhibits excellent salt resistance. The notable water evaporation performance and robust salt resistance provide exciting possibilities for achieving ultrafast solar water purification. [Display omitted] • A photothermo-responsive hydrogel solar evaporator was developed, exhibiting high evaporation rates and salt resistance. • In natural sunlight, the hydrogel autonomously generates a Janus structure through inherent light-temperature responsive. • At night, the evaporator absorbs water and dissolves, facilitating the rapid return of highly concentrated brine. [ABSTRACT FROM AUTHOR]

As a common pollutant in the water environment, microcystin leucine arginine (MC-LR) can enter semen and damage the sperm in animals. However, the mechanism by which MC-LR damages human sperm is unclear. Therefore, human sperm samples were obtained from the Henan Provincial Sperm Bank and exposed to different concentrations (0, 1, 10, and 100 μg/L) of MC-LR for 1, 2, 4, and 6 h, to invegest the effects and potential mechanism of MC-LR on sperm. The results showed that MC-LR mainly accumulated in the neck and flagellum of human sperm. Compared to the control group, the sperm capacitation rate and motility were significantly decreased in the 100 μg/L group. After exposure of 100 μg/L of MC-LR, the central microtubule and microtubule doublet of sperm flagellum were blurred, asymmetrical, or even lost. Furthermore, the expression levels of flagellin DNAH17, SPEF2, SPAG16, SPAG6, and CFAP44 in human sperm were reduced. Also, the phosphorylation levels of CaMKKβ and AMPK can be inhibited by MC-LR. These findings revealed that MC-LR can induce functional and structural damage in human sperm, and the Ca2+/CaMKKβ/AMPK pathway may be involved in this process. This study will provide a basis for prevention and treatment of male fertility declines caused by MC-LR. [Display omitted] • MC-LR mainly accumulates in the neck and flagellum of human sperm • MC-LR decreases the viability, motility, and capacitation of human sperm • MC-LR disrupts the microtubular doublets and central microtubules of the flagellum • The Ca2+/CaMKKβ/AMPK pathways is involved in MC-LR-induced sperm damage [ABSTRACT FROM AUTHOR]

Microcystin-LR (MC-LR), one of aquatic environmental contaminants with reproductive toxicity produced by cyanobacterial blooms, but its toxic effects and mechanisms on the ovary are not fully understood. Here, proteomic techniques and molecular biology experiments were performed to study the potential mechanism of MC-LR-caused ovarian toxicity. Results showed that protein expression profile of ovarian granulosa cells (KK-1) was changed by 17 μg/mL MC-LR exposure. Comparing with the control group, 118 upregulated proteins as well as 97 downregulated proteins were identified in MC-LR group. Function of differentially expressed proteins was found to be enriched in pathways related to adherent junction, such as cadherin binding, cell-cell junction, cell adhesion and focal adherens. Furthermore, in vitro experiments, MC-LR significantly downregulated the expression levels of proteins associated with adherent junction (β-catenin, N-cadherin, and α-catenin) as well as caused cytoskeletal disruption in KK-1 cells (P < 0.05), indicating that the adherent junction was damaged. Results of in vivo experiments have shown that after 14 days of acute MC-LR exposure (40 μg/kg), damaged adherent junction and an increased number of atretic follicles were observed in mouse ovaries. Moreover, MC-LR activated JNK, an upstream regulator of adherent junction proteins, in KK-1 cells and mouse ovarian tissues. In contrast, JNK inhibition alleviated MC-LR-induced adherent junction damage in vivo and in vitro , as well as the number of atretic follicles. Taken together, findings from the present study indicated that JNK is involved in MC-LR-induced granulosa cell adherent junction damage, which accelerated follicular atresia. Our study clarified a novel mechanism of MC-LR-caused ovarian toxicity, providing a theoretical foundation for protecting female reproductive health from environmental pollutants. [Display omitted] • MC-LR exposure can alter the protein expression profile in ovarian granulosa cells. • MC-LR can induce β-catenin degradation in mouse ovarian granulosa cells. • JNK-mediated adherent junction damage is involved in MC-LR-induced follicular atresia. • Inhibition of JNK contributes to alleviating MC-LR-induced ovarian toxicity. [ABSTRACT FROM AUTHOR]

Microcystin-leucine arginine (MC-LR), an emerging water pollutant, produced by cyanobacteria, has an acute testicular toxicity. However, little is known about the chronic toxic effects of MC-LR exposure on the testis at environmental concentrations and the underlying molecular mechanisms. In this study, C57BL/6 J mice were exposed to different low concentrations of MC-LR for 6, 9 and 12 months. The results showed that MC-LR could cause testis structure loss, cell abscission and blood-testis barrier (BTB) damage. Long-term exposure of MC-LR also activated RhoA/ROCK pathway, which was accompanied by the rearrangement of α-Tubulin. Furthermore, MC-LR reduced the levels of the adherens junction proteins (N-cadherin and β-catenin) and the tight junction proteins (ZO-1 and Occludin) in a dose- and time-dependent way, causing BTB damage. MC-LR also reduced the expressions of Occludin, ZO-1, β-catenin, and N-cadherin in TM4 cells, accompanied by a disruption of cytoskeletal proteins. More importantly, the RhoA inhibitor Rhosin ameliorated these MC-LR-induced changes. Together, these new findings suggest that long-term exposure to MC-LR induces BTB damage through RhoA/ROCK activation: involvement of tight junction and adherens junction changes and cytoskeleton disruption. This study highlights a new mechanism for MC-LR-induced BTB disruption and provides new insights into the cause and treatment of BTB disruption. [Display omitted] • This study evaluates the chronic reproductive toxicity of microcystin-leucine arginine (MC-LR). • MC-LR causes blood-testis barrier (BTB) disruption by RhoA/ROCK. • MC-LR induces BTB disruption by adherens junction and tight junction disruption. • MC-LR caused-cytoskeletal rearrangement contributes to BTB disruption. • MC-LR has not only a dose effect but also a time effect on testicular toxicity. [ABSTRACT FROM AUTHOR]

Microcystin-LR (MC-LR) is an intracellular toxin with multi-organ toxicity and the testis is one of its important target organs. Although there is increasing research on MC-LR in male reproductive toxicity, the association between DNA damage and autophagy induced by MC-LR in male germ cells are still unclear. Therefore, it is important to explore the mechanism of MC-LR-induced DNA damage and the role of the activated ATM/p53 signaling pathway in testicular toxicity. The present study showed that MC-LR exposure significantly reduced gonadal index and induced pathological damage of the testes in mice. In addition, MC-LR increased the oxidative stress-related indicator hydroxyl radical, accompanied by increased levels of DNA damage-related indicators gamma-H2AX, 8-hydroxy-2′-deoxyguanosine, the olive tail moment (OTM) and DNA content of comet tail (TailDNA%) in trailing cells. Moreover, MC-LR activated the ATM/p53 pathway by enhancing the phosphorylation levels of ATM, CHK2 and p53 proteins, and then led to cell autophagy, ultimately triggering disrupted testicular cell arrangement, reduced sperm count and spermatogenic cell shedding. Importantly, after pretreatment with the antioxidant NAC, the expression levels of DNA damage-related indicators and the extent of damage in male germ cells were significantly reduced. Furthermore, pretreatment with the ATM inhibitor KU55933 could reduce the occurrence of autophagy and mitigate testicular toxicity of MC-LR through inhibiting the activation of the ATM/p53 pathway. These results indicate that MC-LR-induced oxidative stress can activate the DNA damage-mediated ATM/p53 signalling pathway to induce autophagy in male germ cells. This study provides a novel insight to further clarify the reproductive toxicity caused by MC-LR and to protect male reproductive health. [Display omitted] • MC-LR induces DNA damage in male germ cells. • The ATM/p53 pathway mediated by DNA damage promotes autophagy. • The oxidative stress is involved in MC-LR-induced DNA damage. [ABSTRACT FROM AUTHOR]

As an emerging pollutant in the aquatic environment, microcystin-LR (MC-LR) can enter the body through multiple pathways, and then induce apoptosis and gonadal damage, affecting reproductive function. Previous studies focused on male reproductive toxicity induced by MC-LR neglecting its effects on females. The apoptotic signal-regulated kinase 1 (ASK1) is an upstream protein of P38/JNK pathway, closely associated with apoptosis and organ damage. However, the role of ASK1 in MC-LR-induced reproductive toxicity is unclear. Therefore, this study investigated the role of ASK1 in mouse ovarian injury and apoptosis induced by MC-LR. After MC-LR exposure, ASK1 expression in mouse ovarian granulosa cells was increased at the protein and mRNA levels, and decreased following pretreatment by antioxidant N-acetylcysteine, suggesting that MC-LR-induced oxidative stress has a regulatory role in ASK1 expression. Inhibition of ASK1 expression with siASK1 and NQDI-1 could effectively alleviate MC-LR-induced mitochondrial membrane potential damage and apoptosis in ovarian granulosa cells, as well as pathological damage, apoptosis and the decreased gonadal index in ovaries of C57BL/6 mice. Moreover, the P38/JNK pathway and downstream apoptosis-related proteins (P-P38, P-JNK, P-P53, Fas) and genes (MKK4 , MKK3 , Ddit3 , Mef2c) were activated in vivo and vitro , but their activation was restrained after ASK1 inhibition. Data presented herein suggest that the ASK1-mediated P38/JNK pathway is involved in ovarian injury and apoptosis induced by MC-LR in mice. It is confirmed that ASK1 has an important role in MC-LR-induced ovarian injury, which provides new insights for preventing MCs-induced reproductive toxicity in females. [Display omitted] • MC-LR upregulates ASK1 expression via oxidative stress in mouse ovarian cells. • Inhibition of ASK1 alleviates MC-LR-induced ovarian injury and apoptosis in mice. • ASK1-mediated P38/JNK pathway is involved in MC-LR-induced ovarian injury and apoptosis. • ASK1 activates the P38/JNK pathway via MKK3/4 after ovarian cells exposed to MC-LR. [ABSTRACT FROM AUTHOR]

Wanshan is a city in southwest China that has several inactive mercury (Hg) mines. The local population are exposed to methylmercury (MeHg) due to the consumption of Hg contaminated rice. The relationship between Hg exposure and the cognitive functions of local children is unknown. This study investigated the relationship between hair Hg concentrations and the intelligence quotient (IQ) of 314 children aged 8–10 years, recruited from three local primary schools in Wanshan area in 2018 and 2019. IQ was evaluated using Wechsler Intelligence Scale for Children – Fourth Edition (WISC-IV). The average THg concentration in children's hair samples was 1.53 μg g−1 (range: 0.21–12.6 μg g−1), and 65.6% exceeded the United States Environment Protection Agency (USEPA) recommended value of 1 μg g−1. Results of logistic regression analysis showed that children with hair Hg ≥ 1 μg g−1 were 1.58 times more likely to have an IQ score <80, which is the clinical cut-off for borderline intellectual disability (R2 = 0.20, p = 0.03). Increasing of 1 μg g−1 hair Hg resulted in 1 point of IQ loss in Wanshan children, which was.much higher than that via fish consumption. The economical cost due to Hg exposure was estimated to be $69.8 million (9.43% of total GDP) in the Wanshan area in 2018. Image 1 • Hair Hg in Wanshan children averaged at 1.53 μg g−1. • Children with hair Hg ≥ 1 μg g−1 were 1.58 times more likely to have an IQ score <80. • Increasing of 1 μg g−1 hair Hg resulted in 1 point of IQ loss in Wanshan children. • The economical cost due to Hg exposure was estimated to be $69.8 million (9.43% of total GDP) in the Wanshan area in 2018. [ABSTRACT FROM AUTHOR]