Glufosinate is a common herbicide with neurotoxic effects, leading to seizures, convulsions and memory loss. Glufosinate indirectly induces glutamate toxicity by inhibiting glutamine synthesis in astrocytes. Here, we studied the acute toxic effects of a glufosinate-based herbicide in rat optic nerve at three doses (40, 80 or 120 μM, equal to 714 or 21 mg/kg bw/day). Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), urea, glucose, calcium, as well as creatinine concentrations were analyzed after 24, 48 and 72 h treatment. Intraocular pressure (IOP) (expressed as the average of both eyes) was measured with a rebound tonometer. Interleukin-1β (IL-1β) and c-Fos expression were determined by immunohistochemistry. The results established that the glufosinate-based herbicide significantly increased IL-1β and c-Fos immunopositivity in the optic nerve (p < 0.05), concomitant with increased IOP. These results suggest that commercial formulations of glufosinate acutely affect the optic nerve.
Probiotics are "live", beneficial microbes that provide important health benefits in their hosts. There is significant interest in the modulation and regulation of the immune function by probiotics.To investigate the immunomodulatory effects of a probiotic mixture, including Lactobacillus and Bifidobacterium species, by detecting serum cytokine and immunoglobulin levels.The rats were randomly divided into 4 groups. The first group was "Control group" and other 3 groups were probiotic application groups who received different doses of probiotics. The probiotic mixture included 12 probiotic bacteria, mostly Lactobacillus and Bifidobacterium strains. Probiotic mixture was administered to rats for 12 consecutive days. TNF-α, TGF-β, IL-1-β, IL-6, and IL-10 levels as well as serum IgG and IgA concentrations were detected in the sera after 12 days.Probiotics led to a decrease in the levels of TNF-α, IL-6 and TGF-β; however, they led to increase in the serum levels of IL-10, IgG and IgA. There were significant differences between control group and probiotic application groups (p<0.05).These data suggest that the commensal microbiota are important for stimulating both proinflammatory and regulatory responses in order to rapidly clear infections and minimize inflammation-associated tissue damage.
Benzene, a well-known carcinogenic airborne pollutant, poses significant health risks, particularly in industries such as petroleum, shoemaking, and painting. Despite strict regulations, chronic occupational exposure persists, contributing to the onset of acute myeloid leukemia (AML) and other malignancies. Benzene’s carcinogenicity stems from its metabolic activation, leading to increased oxidative stress, DNA damage, and cancer transformation. While its toxicity is well-documented, the link between genetic and epigenetic alterations and cancer susceptibility in exposed workers remains underexplored. This study aims to identify early biomarkers of benzene exposure and AML risk by analyzing gene expression and DNA methylation datasets from GEO DataSets, integrated with molecular pathway analyses, as well as miRNA-target and protein-protein network evaluations. This multi-approach led to the identification of nine deregulated genes (CRK, CXCR6, GSPT1, KPNA1, MECP2, MELTF, NFKB1, TBC1D7, ZNF331) in workers exposed to benzene, with NFKB1 showing strong discriminatory potential. Also, dose-dependent DNA methylation changes were observed in CXCR6 and MELTF, while selected miRNAs such as let-7d-5p, miR-126-3p, and miR-361-5p emerged as key post-transcriptional regulators. Furthermore, functional enrichment linked these genes to immune response, inflammation, cell proliferation, and apoptosis pathways. While network analyses highlighted NFKB1, CRK, and CXCR6 as central to benzene-associated leukemogenesis. Altogether, these findings provide novel insights into an early biomarker fingerprint for benzene exposure and AML susceptibility, supporting the future development of biomolecular-based targeted occupational health monitoring and personalized preventive strategies for at-risk workers.
INTRODUCTION: There are several type of pesticides to control pests and several new type of pesticides come into use that could less toxic compared to old ones.Pesticide induced oxidative stress which is one of the main mechanism of toxicity, mostly focused research area in the last decade.There are several different studies in the literature on whether pesticide exposure induce oxidative stress parameters mediated toxicity... Pesticide induced oxidative stress level depends on biochemical feature of mammalian systems.Imidacloprid is a neonicotinoid pesticide which widely use that considered safe, however it has been reported in different studies that imidacloprid may cause changes oxidative stress parameters.METHODS: Thus, in this study we aimed to investigate dose and time dependent imidaclopride effects on AcHE, LDH and GSH levels in L-929 fibroblast cell line.1-500 μg imidaclopride dose range effects on acetylcholinesterase, glutathione and lactat dehidrogenase were investigated in this study.RESULTS: LDH levels were significantly increased dose dependently in 250 and 500 ng imidaclopride compared to control group.GSH levels non-significantly decreased dose dependently and GSH levels were decreased in 500 ng imidaclopride group compared to control.There were no significant difference between groups for acetylcholinesterase levels.DISCUSSION AND CONCLUSION: These results indicated that high doses imifoclopride may induce oxidative stress parameters in fibroblast cells.
