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The involved pathways and mechanisms were also explored and discussed.Rodents are the most common models in studies of alcoholic liver disease (ALD). Although several rodents ALD models have been established and multiple mechanisms have been elucidated based on them, these models have some non-negligible shortcomings, specifically only inducing early stage (mainly steatosis, slight to moderate steatohepatitis) but not the whole spectrum of human ALD. The resistance of rodents to advanced ALD has been suggested to be due to the physiological differences between rodents and human beings. Previous studies have reported significant interstrain differences in the susceptibility to ethanol-induced liver injury and in the manifestation of ALD (such as different alteration of lipid profiles). Epigenetic inhibitor order Therefore, it would be interesting to characterize the manifestation of ethanol-induced liver damage in various rodents, which may provide a recommendation to investigators of ALD. Furthermore, more severe ALD models need to be established for the study of serious ALD forms, which may be achieved by using genetic modified rodents.The titanium dioxide nanoparticles (NPs) have been applied to biomedical, pharmaceutical, and food additive fields. However, the effect on health and the environment are conflicting; thus, it has been reviewing several times. In this context, establishing standard robust protocols for detecting cytotoxicity and genotoxicity of nanomaterials became essential for nanotechnology development. The cell type and the intrinsic characteristics of titanium dioxide NPs can influence nanotoxicity. In this work, the cyto- and genotoxicity effects of standard reference material titanium dioxide NPs in primary bovine fibroblasts and immortalized Chinese hamster ovary epithelial (CHO) cells were determined and compared for the first time. Titanium dioxide NPs exposure revealed no cytotoxicity for primary bovine fibroblasts, while only higher concentrations tested (10 μg/ml) induce genotoxic effects in this cell model. In contrast, the lower concentrations of the titanium dioxide NPs cause the cyto- and genotoxic effects in CHO cells. Therefore, our finding indicates that the CHO line was more sensitive toward the effects of titanium dioxide NPs than the primary bovine fibroblast, which should be valuable for their environmental risk assessment.This investigation was conducted to evaluate the effects of clothianidin, a neonicotinoid insecticide, on hepatic oxidative stress biomarkers, biochemical indices of blood serum and liver integrity in juvenile Oncorhynchus mykiss following 7, 14 and 21 days of application to environmentally relevant concentrations of 3, 15 and 30 μg/l. The observed hypertrophy caused elevation in hepatosomatic index, a significant increase in serum glucose and a decrease in tissue protein level with extended period of exposure were determined. The treatment resulted in a marked induction in the activities of antioxidant enzymes which were accompanied with simultaneous elevation in MDA and protein carbonyl level reflecting loss of membrane integrity and protein function. Histopathological examination showed liver injury manifested as hepatocellular degeneration, fibrosis, vacuolation, congestion, necrosis, steatosis and pyknosis proceding with the concentration. The stressful condition triggered hyperglycemic and hypoproteinemic conditions which might be proposed as general adaptive response. Moreover, altered liver histology reveals the hepatotoxic potential of clothianidin via oxidative stress as a common pathological mechanism leading to liver injury.This study aimed to investigate the inhibition activities of lupeol on carbohydrate digesting enzymes and its ability to improve postprandial hyperglycemia in streptozotocin (STZ)-induced diabetic mice. α-Glucosidase and α-amylase inhibitory assays were executed using a chromogenic method. The effect of lupeol on hyperglycemia after a meal was measured by postprandial blood glucose in STZ-induced diabetic and normal mice. The mice were treated orally with soluble starch (2 g/kg BW) alone (control) or with lupeol (10 mg/kg BW) or acarbose (10 mg/kg BW) dissolved in water. Blood samples were taken from tail veins at 0, 30, 60, and 120 min and blood glucose was measured by a glucometer. Lupeol showed noticeable inhibitory activities on α-glucosidase and α-amylase. The half-maximal inhibitory concentrations (IC50) of lupeol on α-glucosidase and α-amylase were 46.23 ± 9.03 and 84.13 ± 6.82 μM, respectively, which were more significantly effective than those of acarbose, which is a positive control. Increase in postprandial blood glucose level was more significantly lowered in the lupeol-administered group than in the control group of both STZ-induced diabetic and normal mice. In addition, the area under the curve was significantly declined with lupeol administration in the STZ-induced diabetic mice. These findings suggest that lupeol can help lower the postprandial hyperglycemia by inhibiting carbohydrate-digesting enzymes.Silicosis is a scarring lung disease caused by inhaling fine particles of crystalline silica in the workplace of many industries. Due to the lack of effective treatment and management, the continued high incidence of silicosis remains a major public health concern worldwide, especially in the developing countries. Till now, related molecular mechanisms underlying silicosis are still not completely understood. Multiple pathways have been reported to be participated in the pathological process of silicosis, and more complex signaling pathways are receiving attention. The activated extracellular signal-regulated kinase (ERK) signaling pathway has been recognized to control some functions in the cell. Recent studies have identified that the ERK signaling pathway contributes to the formation and development of silicosis through regulating the processes of oxidative stress, inflammatory response, proliferation and activation of fibroblasts, epithelial-mesenchymal transformation, autophagy, and apoptosis of cells. In this review article, we summarize the latest findings on the role of ERK signaling pathway in silica-induced experimental models of silicosis, as well as clinical perspectives.