When an organism is exposed to various toxicants chronically, reactive oxygen species(ROS) are accumulated and eventually result in several biological effects from gene expression to cell death. In the present study we investigated the oxidative damage of 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin(TCDD) and/or benzo(a)pyrene (B(a)P) in C100 cells. C100 cells treated with TCDD(30 nM) and B(a)P(3 μM) underwent diverse oxidative stress as determined through thiobarbituric acid-reactive substances(TBARS) formation, DNA fragmentation, DNA single strand break(SSB) assay, immunohistochemical staining of 8-hydroxy-2'-deoxyguanosine(8-OHdG), and mRNA expressions of antioxidant enzymatic genes such as Cu/Zn-SOD gene, GPx(glutathione peroxidase 5) gene, and catalase gene.

A three-month-old, intact male Maltese dog was presented to the hospital with lethargy after taking a human medication, Motilitone. Physical examination, including a neurological examination, revealed no remarkable findings, but cholinergic crisis symptoms appeared gradually. Blood and radiological examinations showed no remarkable findings. The dog was tentatively diagnosed with a cholinergic crisis associated with Motilitone intake. Treatment included intravenous administration of atropine (0.02 mg/kg) every 30 minutes and supportive fluid therapy. After 12 hours of treatment, the patient’s clinical signs were resolved. This is the first case report describing Motilitone toxicity in a dog.

This study was investigated the change of concentration and toxicity of thermally cross-linked superparamagnetic iron oxide nanoparticles (TCL-SPION) on tissues of Sprague-Dawley rats. TCL-SPION at the dose of 15 mg/kg body weight was intravenously injected into the tail vein of the male Sprague-Dawley rats. The fate of TCL-SPION in serum, urine and tissues was observed during 28 days. Serum iron level was maximal at 0.25 h post-injection and gradually declined thereafter. In addition, the sinusoids of liver and the red pulp area of spleen were mainly accumulated iron from 0.5 h to 28-day post-injection. In kidney, iron deposition was detected in the tubular area until 0.5 h after injection. Malondialdehyde concentration in the liver slightly increased with time and was not different with that at zero time. In the liver and spleen, TNF-¥�and IL-6 levels of TS treated with TCL-SPION were not different with those of the control during the experimental period. From the results, TCL-SPION could stay fairly long-time in certain tissues after intravenous injection without toxicity. The results indicated that TCL-SPION might be useful and safe as a contrast for the diagnosis of cancer or a carrier of therapeutic reagents to treat diseases.

The present study was performed to evaluate the relationship between the neurotoxicity of acrylamide and the differential gene expression pattern in mice. Both locomotor test and rota-rod test showed that the group treated with higher than 30 mg/kg/day of acrylamide caused impaired motor activity in mice. Based on cDNA microarray analysis of mouse brain, myelin basic protein gene, kinesin family member 5B gene, and fibroblast growth factor (FGF) 1 and its receptor genes were down-regulated by acrylamide. The genes are known to be essential for neurofilament synthesis, axonal transport, and neuro-protection, respectively. Interestingly, both FGF 1 and its receptor genes were down-regulated. Genes involved in nucleic acid binding such as AU RNA binding protein/enoyl-coA hydratase, translation initiation factor (TIF) 2 alpha kinase 4, activating transcription factor 2, and U2AF 1 related sequence 1 genes were down-regulated. More interesting finding was that genes of both catalytic and regulatory subunit of protein phosphatases which are important for signal transduction pathways were down-regulated. Here, we propose that acrylamide induces neurotoxicity by regulation of genes associated with neurofilament synthesis, axonal transport, neuro-protection, and signal transduction pathways.

The aim of the present study was to determine the acute and subacute potential of trichlorfon in guppies (Poecilia reticulata). We first defined the 24h median tolerance limit (TLm∧24h) of the fish to trichlorfon. Guppies were then treated with TLm∧24h and 1/10 TLm∧24h trichlorfon concentrations to evaluate of any histological alterations occurred. The TLm∧24h value of trichlorfon was 11 ppm. This concentration resulted in acute toxicity to the gills and kidneys with edema, hyperplasia of the gill lamellae, and vacuolated degeneration and necrosis of renal tubular cells. In the case of subacute toxicity using a 10-fold dilution of the TLm∧24h value (1.1 ppm), no behavioral changes, external lesions or histopathological changes were observed. Therefore, safe concentration of trichlorfon might be 1.1 ppm in guppy for controlling parasitic infections.