Sutherlandnicolaisen8464

Arsenic (As) toxicity is a problem that needs to be solved in terms of both human health and agricultural production in the vast majority of the world. The presence of As causes biomass loss by disrupting the balance of biochemical processes in plants and preventing growth/water absorption in the roots and accumulating in the edible parts of the plant and entering the food chain. A critical method of combating As toxicity is the use of biosafe, natural, bioactive compounds such as hesperidin (HP) or chlorogenic acid (CA). To this end, in this study, the physiological and biochemical effects of HP (100 μM) and CA (50 μM) were investigated in Zea mays under arsenate stress (100 μM). Relative water content, osmotic potential, photosynthesis-related parameters were suppressed under stress. It was determined that stress decreased the activities of the antioxidant system and increased the level of saturated fatty acids and, gene expression of PHT transporters involved in the uptake and translocation of arsenate. Afry and preserving the biochemical reactions of photosynthesis.In this study, the organ distribution and exposure risk from dietary intake of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) were investigated for lotus collected from Ya-er Lake, a lake in Hubei Province, Central China that was historically polluted by the chlor-alkali industry. The highest concentrations of PCDD/Fs were found in the main and fibrous lotus roots, with mean values of 48.9 ± 90.1 pg/g and 94.6 ± 143 pg/g, respectively. In all the investigated samples, Octa-CDD (OCDD) and Octa-CDF (OCDF) were the predominant congeners, at 26% and 17% of Σ17 PCDD/Fs, respectively, followed by 1,2,3,4,6,7,8-HpCDF (9%). The distribution ratios of PCDD/Fs in adjacent lotus organs indicated that PCDD/Fs accumulated easily in edible organs, such as lotus seeds, membrane and leaves. The WHO-TEQ in the edible lotus organs and the probable daily intake (PDI) of lotus products by residents were calculated the toxic equivalents in the lotus fruit parts reached a mean of 2 pg WHO-TEQ2005/g dw, and the mean weekly intake of lotus products for adolescents living around Ya-er Lake was 2.3 pg WHO-TEQ/kg bw/week. These results suggested that long-term consumption of lotus products from Ya-er Lake presents a health hazard to residents.Among the most prevalent sources of biodiversity declines, Artificial Light At Night (ALAN) is an emerging threat to global biodiversity. Much knowledge has already been gained to reduce impacts. However, the spatial variation of ALAN effects on biodiversity in interaction with landscape composition remains little studied, though it is of the utmost importance to identify lightscapes most in need of action. Several studies have shown that, at local scale, tree cover can intensify positive or negative effects of ALAN on biodiversity, but none have - at landscape scale - studied a wider range of landscape compositions around lit sites. We hypothesized that the magnitude of ALAN effects will depend on landscape composition and species' tolerance to light. Taking the case of insectivorous bats because of their varying sensitivity to ALAN, we investigated the species-specific activity response to ALAN. Bat activity was recorded along a gradient of light radiance. We ensured a large variability in landscape composition around 253 sampling sites. Among the 13 bat taxa studied, radiance decreased the activity of two groups of the slow-flying gleaner guild (Myotis and Plecotus spp.) and one species of the aerial-hawking guild (Pipistrellus pipistrellus), and increased the activity of two species of the aerial-hawking guild (Pipistrellus kuhlii and Pipistrellus pygmaeus). Among these five effects, the magnitude of four of them was driven by landscape composition. For five other species, ALAN effects were only detectable in particular landscape compositions, making the main effect of radiance undetectable without account for interactions with landscape. Specifically, effects were strongest in non-urban habitats, for both guilds. Results highlight the importance to prioritize ALAN reduction efforts in non-urban habitats, and how important is to account for landscape composition when studying ALAN effects on bats to avoid missing effects.Dynamic regulation of G-protein-coupled receptor (GPCR) kinase 2 (GRK2) expression restores cellular function by protecting from overstimulation via GPCR and non-GPCR signaling. In the primary afferent neurons, GRK2 negatively regulates nociceptive tone. The present study tested the hypothesis that induction of GRK2 in the primary afferent neurons contributes to the resolution of acute pain after tissue injury. GRK2 expression in the dorsal root ganglion (DRG) was analyzed at 1 and 7 days after the incision. Intraperitoneal administration of a GRK2 inhibitor was performed 7 days post-incision in male Sprague-Dawley rats who underwent plantar incisions to analyze the pain-related behavioral effect of the GRK2 inhibitor. Separately, GRK2 expression was analyzed after injecting insulin-like growth factor 1 (IGF1) into the rat hind paw. In addition, an IGF1 receptor (IGF1R) inhibitor was administered in the plantar incision rats to determine its effect on the incision-induced hyperalgesia and GRK2 expression. Plantar incision induced an increase in GRK2 in the DRG at 7 days, but not at 1 day post-incision. Acute hyperalgesia after the plantar incision disappeared by 7 days post-incision. Intraperitoneal injection of the GRK2 inhibitor at this time reinstated mechanical hyperalgesia, although the GRK2 inhibitor did not produce hyperalgesia in naive rats. After the incision, IGF1 expression increased in the paw, but not in the DRG. Intraplantar injection of IGF1 increased GRK2 expression in the ipsilateral DRG. IGF1R inhibitor administration prevented both the induction of GRK2 and resolution of hyperalgesia after the plantar incision. These findings demonstrate that induction of GRK2 expression driven by tissue IGF1 has potent analgesic effects and produces resolution of hyperalgesia after tissue injury. Dysregulation of IGF1-GRK2 signaling could potentially lead to failure of the spontaneous resolution of acute pain and, hence, development of chronic pain after surgery.Galaxolide and tonalide are well-known polycyclic musks whose intensive use without limitations in numerous cleaning, hygiene, and personal care products has resulted in widespread direct human exposure via absorption, inhalation, and oral ingestion. Latest data shows that long-term, low-dose exposure to toxic chemicals can induce unpredictable harmful effects in a variety of living systems, however, interactions between synthetic musks and brain tumours remain largely unexplored. Glioblastoma (GB) accounts for nearly half of all tumours of the central nervous system and is characterized by very poor prognosis. The aims of this study were (1) to investigate the potential effect of long-term (20-generation) single and combined application of galaxolide and tonalide at sub-lethal doses (5-2.5 u M) on the angiogenesis, invasion, and migration of human U87 cells or tumour spheroids, and (2) to explore the underlying molecular mechanisms. Random amplified polymorphic DNA assays revealed significant DNA damage and a therapy regime. Additionally, we recommend that extensively-used hygiene and cleaning materials be selected from synthetic musk-free products, especially when used in palliative care processes for GB patients.This study explores the effect of acute Ethanol (EtOH) exposure on Bone Morphogenetic Protein (BMP)-evoked intracellular signaling, and the concomitant morphological changes induced by EtOH in C2C12 cells and DRG (Dorsal root ganglion) neurons in an in vitro model related to Fetal Alcohol Syndrome Disorder (FASD). All assays were performed within 30 min of BMP stimulation to specifically investigate the earliest events occurring in BMP-evoked intracellular signaling pathways. We show that Smad phosphorylation and nuclear translocation stimulated by BMPs was not altered following acute exposure to EtOH. In contrast, acute EtOH exposure alone caused a striking concentration-dependent decrease in Akt phosphorylation, as well as a loss of adhesion in C2C12 cells. The addition of BMPs before exposure to EtOH was associated with maintenance of Akt phosphorylation, greater cell adhesion in C2C12 cells, and preservation of growth cone complexity in DRG neurons. Thus, for both C2C12 cells and DRG neurons, BMPs, acting through non-canonical BMP signaling pathways, appear to impart some protection against the profound effects of acute EtOH exposure on cellular adhesion and structure.Cylindrospermopsin (CYN) is a toxic secondary metabolite from cyanobacteria that can cause cardiovascular disease. However, the study of CYN-induced cardiovascular toxicity in vitro is very limited and the mechanism is remain to be clarified. Vascular smooth muscle cells (VMSCs) have an important function in maintaining the structural and functional integrity of the aortic wall, and are an important in vitro model for cardiovascular research. Thus, the effects of CYN exposure (2, 20, 200, and 2000 nM) on VMSCs were analyzed. In vitro study, results showed that CYN exposure decreased VMSCs viability, inhibited VMSCs migration, induced DNA damage, destroyed cytoskeleton, changed cell morphology, promoted VMSCs apoptosis, and increased intracellular reactive oxygen species (ROS) levels. In addition, CYN could induce the activities of SOD, CAT and GPX, and promote the expressions of SOD1, CAT, GPx1, p53 and Bax genes and inhibit the expression of Bcl-2 gene, leading to a higher ratio of Bax/Bcl-2. Taken together, CYN may induce ROS overproduction, leading to increased p53 expression and ultimately promoting VSMC apoptosis. Therefore, the present study demonstrates that CYN could impair VMSCs, leading to vascular developmental defects and angiocardiopathy.In this study, we aimed to elucidate the role of chronic cadmium (Cd) exposure in epithelial-mesenchymal transition (EMT) and thus malignant phenotypic changes of prostate cancer cells. Crenolanib datasheet Prostate cancer cells (PC-3 and DU145) were exposed to a non-toxic level (0.5 or 2 μM) of Cd for up to 3 months, which resulted in significantly promoted migration and invasion of the cells. These phenotypic changes were considered to be the consequence of enhanced EMT as evidenced by diminished expression of E-cadherin and increased vimentin expression. Regarding the mechanisms of Cd-induced EMT, we found Smad3 was activated but without upregulation of TGF-β. Alternatively, we found endoplasmic reticulum (ER) stress of prostate cancer cells was significantly evoked, which was parallel with the increased reactive oxygen species (ROS). Removal of ROS by N-acetylcysteine significantly reduced ER stress in prostate cancer cells, followed by the decrease of Smad3 phosphorylation and expression of nuclear Snail, resulting in the inhibition of EMT and malignant phenotypic changes of prostate cancer cells. These findings indicated a new TGF-β independent, ROS-mediated ER stress/Smad signaling pathway in chronic Cd exposure-induced EMT of prostate cancer cells, which could be a novel mechanism involved in cadmium-mediated cancer cells malignant transformation. Accordingly, ROS-induced ERs may become a novel preventive and therapeutic target for cancer.