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Acetaminophen is a widely used analgesic that has been detected in many water bodies with few reports concerning its potential toxicity to fish. This study sought to assess the developmental, swimming performance and cardiovascular activities of embryo/larvae catfish (Clarias gariepinus) exposed to acetaminophen. The Organization for Economic Development (OECD) Fish Embryo Acute Toxicity Test (OECD 236) was employed. Fertilized embryo were exposed to different concentrations of acetaminophen (0, 0.5, 1, 10 µg/L) for 96 h. Hatching rates of the embryo were observed to decrease with increasing concentrations of acetaminophen. Fish embryo exposed to acetaminophen displayed varying levels of teratogenic effects at different levels of development in a dose-dependent manner. The results also showed a significant (p less then 0.05) dose-dependent increase in swimming speed and movement patterns in fish larvae exposed to acetaminophen, with distance travelled in larvae exposed to the highest concentration of acetaminophen (10 µg/L) about eight (8) times the distance travelled by the control larvae, indicating that acetaminophen-induced erratic swimming behaviour in the catfish species. Cardiotoxicity was evident, with a significant reduction in heartbeat rate with increasing concentrations of acetaminophen. The results showed that exposure to acetaminophen resulted in teratogenic, neurotoxic and cardiotoxic effects in embryo/larvae of Clarias gariepinus. The findings suggest that acetaminophen which has recently been detected in many water bodies could potentially impact on survival of aquatic life, especially catfish.<br /><br /> Gender difference and PM<br /><br /> exposure all have effects on hypertension, change of estrogen level in different women's stage bring complex influence on blood pressure. [https://www.selleckchem.com/products/d-4476.html selleck chemicals llc] Then we conduct this meta-analysis to investigate the association between long-term exposure (at least one year) to fine particulate matter (PM<br /><br /> ) and hypertension in adult non-pregnant women.<br /><br /> Four major databases PubMed, Cochrane Library, Web of Science and Embase were searched with specific search terms, and 11 studies were finally selected. The meta-analysis module of software Stata 12.0 was used for data processing with the effect values hazard ratio (HR) and odds ratio (OR) respectively.<br /><br /> After sensitivity analysis, we removed a study with highly heterogeneity and finally included 10 studies. Meta-analysis results showed that exposure to PM<br /><br /> (per 10μg/m<br /><br /> increase) was associated with hypertension in non-pregnancy adult women, HR =1.23, 95%CI 1.08-1.40; OR =1.07, 95%CI 1.00-1.14. And subgroup analysis showed that menopause, non-White and diabetes are the key risk factors of hypertension when exposed to PM<br /><br /> .<br /><br /> This is the first meta-analysis to explore the association between PM<br /><br /> and non-pregnancy women, and calculate OR and HR respectively for the first time. Exposure to PM<br /><br /> could increase the risk of hypertension in non-pregnancy women, and the combined 'HR' was much higher than 'OR'.<br /><br />This is the first meta-analysis to explore the association between PM2.5 and non-pregnancy women, and calculate OR and HR respectively for the first time. Exposure to PM2.5 could increase the risk of hypertension in non-pregnancy women, and the combined 'HR' was much higher than 'OR'.Reducing the potential leaching of Mo and Ni from the fly ash (FA) of petroleum coke is an increasingly important issue as Asia and Europe's demand is expected to drastically intensify as continuing urbanisation and technological innovation demands ever more electricity. In the present study, we investigated coal combustion products (CCP) from a large coal-fired power station fed with a 5644 coal/petroleum coke blend. Results revealed that leachable concentrations of Mo and Ni from FA were in the upper non-hazardous limit and in the inert limit, respectively (2003/33/EC). Whilst common prevention measures for Mo and Ni based on the adsorption capacity of boiler slag (BS), a mixture of BS goethite, and jarosite, were considered insufficient to reduce the potential leaching of Mo into FA leachates, a novel chemical stabilisation method based on an aggregate product of portlandite and FA immobilised both Mo and Ni such that the resulting concentrations were below the limits established in the abovementioned 2003 EC Decision. Precipitation may be responsible for the fixation of Mo and Ni in the FA portlandite aggregates as Ca(MoO4) and NiMoO4, respectively. The findings of this novel study support the use of this aggregate to reduce FA pollutants, which will be of particular interest to nations that remain largely coal/petroleum coke-dependant.The base excision repair (BER) pathway is an important defense response to oxidative DNA damage. It is known that exposures to phthalate esters (PAEs), including Dibutyl phthalate (DBP), Mono-(2-ethylhexyl) phthalate (MEHP), and Di-(2-ethylhexyl) phthalate (DEHP), cause reactive oxygen species-induced DNA damage and oxidative stress. Here, we determined the mRNA levels of BER pathway-related genes (ogg1, nthl1, apex1, parp1, xrcc1, lig3, ung, pcna, polb, pold, fen1, and lig1), pro-apoptotic gene (bax), and apoptotic suppressor gene (bcl2) in different PAEs-exposed zebrafish larvae and HEK293T cells. Further investigations were performed to examine reactive oxygen species (ROS) accumulation, superoxide dismutase (SOD) activity, developmental toxicity, and cell viability after PAEs exposure in vivo and in vitro. The results showed that PAEs exposure can induce developmental abnormalities in zebrafish larvae, and inhibit cell viability in HEK293T cells. Additionally, we found that PAEs exposure results in the accumulation of ROS and the inhibition of SOD activation in vivo and in vitro. Notably, the mRNA levels of BER pathway-related genes (OGG1, NTHL1, APEX1, XRCC1, UNG, POLB, POLD, FEN1) were significantly upregulated after DBP or MEHP exposure, whereas the mRNA levels of NTHL1, UNG, POLB, POLD, and FEN1 were significantly altered in DEHP-treated HEK293T cells. In zebrafish, the mRNA levels of ogg1, pcna, fen1 and lig1 genes were increased after DBP or DEHP exposure, whereas the mRNA levels of nthl1, apex1, parp1, lig3, pcna and polb were decreased after MEHP exposure, respectively. Thus, our findings indicated that PAEs exposure can induce developmental toxicity, cytotoxicity, and oxidative stress, as well as activate BER pathway in vivo and in vitro, suggesting that BER pathway might play critical roles in PAEs-induced oxidative stress through repairing oxidative DNA damage.