We concluded that adding CGA to SILY acts as a hepatoprotective agent against DOX-induced liver injury through inhibiting apoptosis biomarkers, maintaining antioxidant enzyme levels, decreasing pro-inflammatory cytokines as well as regulating liver adenosine monophosphate-activated protein kinase signaling.The respiratory tract and the oral mucosa are the first areas contaminated by pesticides. The herbicide dichlorophenoxyacetic acid (2,4-D) is a widely used pesticide across the world for both crops and gardens. The aim of this study was to evaluate oral mucosal damage after an experimental simulation of chronic oral and inhalational environmental exposure to 2,4-D formulation. Eighty male Wistar rats were exposed to three distinct concentrations of 2,4-D formulation (low-187.17 mg/m3; medium-313.31 mg/m3; and high-467.93 mg/m3). Oral exposure (through contaminated feed) or inhalation exposure lasted 6 months. Rat tongues were collected for cyto- and histopathology. There was a difference between exposure groups in the intensity of tissue congestion. Most rats exposed to 2,4-D presented mucosal inflammation at both cytology and histology (P less then 0.05). Hyperkeratosis only occurred in rats exposed orally at the high concentration. There was an increase in the number of nucleoli-organizing regions in the dorsal epithelium as the 2,4-D concentration increased (P less then 0.001). The inhalation route was more associated with increased mitosis figures and nucleoli-organizing region count (P less then 0.05). Chronic oral and inhalation exposure to high concentrations of 2,4-D formulation caused an increase in the proliferation rate and thickness of the tongue epithelium and stimulated the inflammatory response in the tissue.Lake Van fish (Alburnus tarichi Guldenstadt 1814) is the only fish that can adapt to the extreme conditions (pH 9.8 salinity 0.2% and alkalinity 151.2 meq/L) of Lake Van. In this study, it was aimed to determine the cytotoxic and genotoxic effects of chlorpyrifos (CPF) on Lake Van fish primary gill cell culture. Gill epithelium from Lake Van fish was isolated enzymatically and grown in primary culture on Leibovitz's L-15 medium. After different doses (0.01, 0.1, 1, and 10 μM) of CPF were applied to the gill cells, the total oxidant status (TOS), total antioxidant status (TAS), malondialdehyde (MDA), and DNA damage levels (8-hydroxyguanine (8-OHdG)) were examined at the end of 24 and 48 h. It was determined that the TOS, MDA, and 8-OHdG levels increased in the cells exposed to high doses (1 and 10 μM) of CPF and the TAS was decreased (P less then 0.05). It was revealed from this study that CPF administered at a dose higher than 1 μM can cause oxidative stress and DNA damage in the primary gill cell culture of Lake Van fish. In addition, the findings showed that Lake Van fish primary gill cell culture was useful in determining the effects of toxic substances likely to be the contaminants of a lake. JWH-018 was the first synthetic cannabinoid introduced as a legal high and the first of the new generation of novel psychoactive substances that flooded worldwide drug markets. JWH-018 was marketed as "spice," "herbal incense," or "herbal blend," as a popular and legal (at the time) alternative to cannabis (marijuana). JWH-018 is a potent synthetic cannabinoid with considerable toxicity associated with its use. JWH-018 has qualitatively similar but quantitatively greater pharmacological effects than cannabis, leading to intoxications and even deaths. The mechanisms of action of the drug's toxicity require research, and thus, the aim of the present study was to investigate the toxicological profile of JWH-018 in human SH-SY5Y neuronal cells. SH-SY5Y neuronal cells were exposed to increasing concentrations from 5 to 150μM JWH-018 over 24h. Cytotoxicity, DNA damage, the apoptotic/necrotic rate, and oxidative stress were assessed following SH-SY5Y exposure. JWH-018 did not produce a significant decrease in SH-SY5Y cell viability, did not alter apoptotic/necrotic rate, and did not cause genotoxicity in SH-SY5Y cells with 24-h exposure. Glutathione reductase and catalase activities were significantly reduced; however, there was no significant change in glutathione peroxidase activity. Also, JWH-018 treatment significantly decreased glutathione concentrations, significantly increased protein carbonylation, and significantly increased malondialdehyde (MDA) concentrations. For significance, all <0.05. JWH-018 produced oxidative stress in SH-SY5Y cells that could be an underlying mechanism of JWH-018 neurotoxicity. Additional animal and human-based studies are needed to confirm our findings.JWH-018 produced oxidative stress in SH-SY5Y cells that could be an underlying mechanism of JWH-018 neurotoxicity. Additional in vivo animal and human-based studies are needed to confirm our findings.Wernicke's encephalopathy (WE) is an acute neuropsychiatric state. Untreated, WE can lead to coma or death, or progress to Korsakoff syndrome (KS) - a dementia characterized by irreversible loss of anterograde memory. Thiamine (vitamin B1) deficiency lies at the heart of this condition. Yet, our understanding of thiamine regarding prophylaxis and treatment of WE remains limited. selleck chemicals llc This may contribute to the current undertreatment of WE in clinical practice. The overall aim of this review is to identify the best strategies for prophylaxis and treatment of WE in regard to (a) dose of thiamine, (b) mode of administration, (c) timing of switch from one mode of administration to another, (d) duration of administration, and (e) use of magnesium along thiamine as an essential cofactor. Evidence from randomized controlled trials and other intervention studies is virtually absent. Therefore, we have to resort to basic science for proof of principle instead. Here, we present the first part of our clinical review, in which we explore the physiology of thiamine and the pathophysiology of thiamine deficiency. We first explore both of these in their historical context. We then review the pharmacodynamics and pharmacokinetics of thiamine, exploring the roles of the six currently known thiamine compounds, their transporters, and target enzymes. We also explore the significance of magnesium as a cofactor in thiamine-facilitated enzymatic reactions and thiamine transport. In the second (forthcoming) part of this review, we will use the findings of the current review to make evidence-based inferences about strategies for prophylaxis and treatment of WE.