Bjerringclapp9230

The study investigated the responses of the submerged macrophyte Vallisneria natans (V. natans) to snails (Bellamya aeruginosa) at different densities, with changes in physiological parameters, morphology, leaf-epiphytic bacteria community and water quality parameters examined. The changes of water quality parameters (pH, total nitrogen (TN), total phosphorus (TP) and total organic carbon (TOC)) indicated that snails secreted nutrients into water. Changes in morphological and physiological parameters (fresh weight, root length, shoot height, chlorophyll, malondialdehyde (MDA), activities of superoxide dismutase (SOD), catalase (CAT) and peroxidase (POD)) demonstrated that the presence of snails were beneficial to the growth of submerged macrophytes. Microbial diversity analyses indicated that snails could decrease microbial community richness and diversity. At medium densities (340 ind. m-2), an increase in snail density was beneficial to the growth of submerged macrophytes. The results of this study provide theoretical guidance and technical support for the maintenance and restoration of submerged macrophytes. Tebuconazole, a widely used fungicide, can severely disrupt the reproductive process of various organisms. In this study, we investigated the subacute effects of tebuconazole on the earthworm to fully understand its toxic implications. Herein, untargeted metabolomics, mRNA assay and biochemical approaches were adopted to evaluate the subacute effects of Eisenia fetida earthworms, when exposed to tebuconazole at three different concentrations (0.5, 5 and 50 mg/kg) for seven days. SOD enzyme activity test displayed that tebuconazole exposure interfered with the earthworms' ROS. ANN mRNA expression was down-regulated after tebuconazole exposure. Triptolide mw 1H nuclear magnetic resonance (1H-NMR)-based untargeted metabolomics study showed that 5 mg/kg tebuconazole exposure interfered with earthworms' metabolism. Twelve significantly changed metabolites were identified. The pathway analyses indicate that tebuconazole can disrupt the earthworm's metabolism, particularly in the AMP pathway, which impact the reproduction. This may explain the tebuconazole's mechanism of action behind the down-regulation of the expression of ANN mRNA, which is related to the earthworm's reproductive process. We comprehensively evaluated the mRNA expression, enzyme activity, and metabolomics, and acquired sufficient information for evaluating the toxicity of tebuconazole. Ferroptosis is a newly identified form of cell death characterized by accumulation of intracellular iron and requirement of lipid peroxidation. However, whether arsenite triggers testicular cell death via ferroptosis remains unclear. In this study, after administrating of adult male mice with 0.5, 5 and 50 mg/L arsenite for six months via drinking water, the results showed that arsenite caused the pathological changes in mouse testis and significantly reduced the number of sperm. Mitochondrial injuries were observed as the major ultrastructural damages induced by arsenite, and these damages were accompanied by the apparent mitochondrial oxidative damage in the testis, manifested by accumulation of iron, production of reactive oxygen species and lipid peroxidation products. We also demonstrated that arsenite significantly activated ferroptosis-related signal pathways in the mouse testis. To further verify the results obtained in the animal model, GC-2spd cells were employed as the in vitro culture system. Consistently, the results revealed arsenite remarkably triggered the ferroptotic cell death in vitro, and inhibition of ferroptosis by ferrostatin-1 could attenuate this adverse effect in cells. These findings together indicate that arsenite can trigger oxidative stress thus leading to testicular cell death by ferroptosis, suggesting that inhibition of ferroptosis would be a potential strategy for treatment of arsenite-related male reproductive toxicity. Lead is a toxic metal found in environment with great neurotoxic potential. The main effect is associated with impairments in hippocampus and cerebellum, driving to cognitive and motor dysfunctions, however, there is a lack of evidences about the effects over the spinal cord. In this way, we aimed to investigate in vivo the effects of long-term exposure to lead acetate in oxidative biochemistry and morphology of rats' spinal cord. For this, 36 male Wistar rats (Rattus norvegicus) were divided into the group exposed to 50 mg/kg of lead acetate and control group, which received only distilled water, both groups through intragastric gavage, for 55 days. After the exposure period, the animals were euthanized and the spinal cords were collected to perform the analyses of lead levels quantification, oxidative biochemistry evaluation by levels of malondialdehyde (MDA), nitrites and the antioxidant capacity against peroxyl radicals (ACAP). Besides, morphological evaluation with quantitative analysis of mature and motor neurons and reactivity to myelin basic protein (MBP). Our results showed high levels of lead in spinal cord after long-term exposure; there was a reduction on ACAP level; however, there was no difference observed in MDA and nitrite levels. Moreover, there was a reduction of mature and motor neurons in all three regions, and a reduction of immunolabeling of MBP in the thoracic and lumbar segments. Therefore, we conclude that long-term exposure to lead is able of increasing the levels of the metal in spinal cord, affecting the antioxidant capacity and inducing morphological impairments in spinal cord parenchyma. Our results also suggest that the tissue impairments triggered by lead may be resultant from others molecular mechanisms besides the oxidative stress. For the treatment of low C/N wastewaters, methanol or acetate is usually dosed as electron donor for denitrification but such organics makes the process costly. To decrease the cost, iron which is the fourth most abundant element in lithosphere is suggested as the substitution of methanol and acetate. The peak volumetric removal rate (VRR) of nitrate nitrogen in the ferrous iron-dependent nitrate removal (FeNiR) reactor was 0.70 ± 0.04 kg-N/(m3·d), and the corresponding removal efficiency was 98%. Iron showed toxicity to cells by decreasing the live cell amount (dropped 56%) and the live cell activity (dropped 70%). The toxicity of iron was mainly expressed by the formation of iron encrustation. From microbial community data analysis, heterotrophs (Paracocccus, Thauera and Azoarcus) faded away while the facultative chemolithotrophs (Hyphomicrobium and Anaerolineaceae_uncultured) dominated in the reactor after replacing acetate with ferrous iron in the influent. Through scanning electron microscope (SEM) and transmission electron microscope (TEM), two iron oxidation sites in FeNiR cells were observed and accordingly two FeNiR mechanisms were proposed 1) extracellular FeNiR in which ferrous iron was bio-oxidized extracellularly; and 2) intracellular FeNiR in which ferrous iron was chemically oxidized in periplasm.