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Living organisms have an innate ability to regulate the synthesis of inorganic materials, such as bones and teeth in humans. Cadmium sulfide (CdS) can be utilized as a quantum dot that functions as a unique light-emitting semiconductor nanocrystal. The increased use in CdS has led to an increased inhalation and ingestion rate of CdS by humans which requires a broader appreciation for the acute and chronic toxicity of CdS. We investigated the toxic effects of CdS on cerebellar cell cultures and rat brain. We employed a ‘green synthesis’ biosynthesis process to obtain biocompatible material that can be used in living organisms, such as Viridibacillus arenosi K64. Nanocrystal formation was initiated by adding CdCl2 (1 mM) to the cell cultures. Our in vitro results established that increased concentrations of CdS (0.1 μg/mL) lead to decreased cell viability as assessed using 3-[4,5-dimethylthiazole-2-yl]-2,5-diphenyltetrazolium bromide (MTT), total antioxidant capacity (TAC), and total oxidant status (TOS). The in vivo studies showed that exposure to CdS (1 mg/kg) glial fibrillary acidic protein (GFAP) and 8-hydroxy-2' -deoxyguanosine (8-OHdG) were increased. Collectively, we describe a model system that addresses the process from the synthesis to the neurotoxicity assessment for CdS both in vitro and in vivo. These data will be beneficial in establishing a more comprehensive pathway for the understanding of quantum dot-induced neurotoxicity.

We studied the acute toxicity of an imazamox-based herbicide at 12, 24 and 36 mg/kg body (bw) weight imazamox equivalent dose on the liver and pancreatic tissue in Sprague Dawley rats. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, glucose, calcium as well as creatinine, were determined in blood samples, which were collected after 24, 48 and 72 h exposure. Caspase 3 and anti-insulin expression and immunopositivity were evaluated using in situ hybridization and immunohistochemistry, respectively. The imazamox-based herbicide evaluated in this study induced toxic effects even from the lowest dose tested (12 mg/kg bw). The two highest doses caused a statistically significant cytotoxicity on the Langerhans islet cells. Necrotic and degenerative changes were detected in hepatocytes at the two highest doses. Imazamox is considered to be poorly toxic to the liver. Nevertheless, the imazamox-based herbicide formulation tested here reduced the size of the β-islet cells, induced an elevation in serum glucose and calcium. Our data shows that commercial formulations of imazamox containing various co-formulants can have hepatic and pancreatic toxic effects. Keywords: Anti-insulin, Caspase 3, Imazamox, Immunohistochemistry, In situ hybridization

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