Methylmercury is an environmental pollutant that causes severe central nervous system damage. However, the mechanism involved in its toxicity remains unclear. In this study, expression of thioredoxin-interacting protein (TXNIP), which is involved in the regulation of intracellular redox status, was rapidly induced in mouse neuronal C17.2 cells in response to methylmercury exposure. In addition, C17.2 cells transfected with small interfering RNA against TXNIP mRNA showed greater resistance to methylmercury than control cells. These findings suggest that TXNIP is a novel factor involved in enhancing methylmercury toxicity and that methylmercury may cause cell death by inducing TXNIP expression.

Volatile organic compound 2-ethyl-1-hexanol (2EH) causes the sick building syndrome. Inhalation exposure to 2EH causes olfactory epithelium (OE) degeneration and olfactory neuron loss in mice, which recover temporarily despite continued exposure but subsequently experience similar toxic effects. However, the exact course of recovery after 2EH cessation remains unknown. Therefore, in this study, we aimed to evaluate the histopathological changes in OE after 2EH inhalation cessation. Male ICR mice were exposed to 70 ppm 2EH for 8 hr daily, five days a week, for four weeks, followed by a recovery period of up to four weeks. Histopathological changes in mouse OE on the first (D1) and third (D3) days and first (W1), second (W2), and fourth (W4) weeks of the recovery period were analyzed. Notably, 2EH induced OE degeneration at W2, enlarged the Bowman’s glands at W1 and W2, and decreased the olfactory marker protein-positive cell proportions at W1 and W2. Total leukocytes, neutrophils, and lymphocytes were abundant at both W1 and W2, with no significant differences. Proliferating cell nuclear antigen-positive basal cell number increased; they were distributed throughout the OE on D1 but subsequently lined up the basement membrane and remained at low levels thereafter. Number of growth-associated protein-43-positive immature olfactory neurons increased from D3 to W2. In conclusion, OE was not immediately repaired; the toxic effects appeared 1–2 weeks after 2EH cessation, as indicated by the OE tissue damage with decreased olfactory marker protein-positive cell proportions, followed by proper recovery.

The prevalence of antibiotic residues and antibiotic-resistant bacteria in natural environments due to human and livestock waste emissions, pesticide runoff, and pharmaceutical effluents poses a serious threat to public health. Therefore, in this study, we aimed to examine the characteristics, including antibiotic susceptibility, biofilm formation ability, and virulence genes, of levofloxacin (LVFX)-resistant Escherichia coli isolated from the Tone River. Liquid chromatography-tandem mass spectrometry analysis revealed that the upstream, midstream, and downstream river water samples contained 2.2, 19.5, and 15.7 ng/L LVFX, respectively. Despite the very low concentration of LVFX, LVFX-resistant E. coli were isolated from the midstream and downstream regions. Based on the antibiotic sensitivity patterns, the following representative strains were selected: TLR101 and TLR104 (from midstream) and TLR105 and TLR108 (from downstream). These four isolates were LVFX and multidrug-resistant, with TLR101 showing high resistance to ampicillin and the others showing high resistance to chloramphenicol and tetracycline. Biofilm formation assays revealed that TLR104 and TLR108 exhibit very strong biofilm-forming abilities. One-step multiplex polymerase chain reaction (PCR) assays were used to detect various virulence genes, including eaeA, bfpA, invE, ipaH, stx1, stx2, elt, sth, aggR, and astA. A 100-bp astA gene product was detected in TLR104, and DNA sequence analysis confirmed this amplified PCR product, identifying it as a diarrheagenic E. coli strain. Overall, this study revealed the presence of multidrug-resistant diarrheagenic E. coli in the Tone River, underscoring the need for effective public health measures to prevent the release of untreated sewage and industrial waste into the river.

In repeated dose administration toxicity studies, which are regulatory requirements for the safety evaluation of drugs, pesticides, etc., the analysis of between-group differences is typically carried out using either parametric or nonparametric statistical methods. The choice of the method depends on whether the data distributions within the groups are normal or not, and or are homogeneous. In theory, testing for normality is important because many parametric tests, such as the t-test and ANOVA, assume that the data within each group follows a normal distribution. However, in repeated dose administration toxicity studies, the data are not always explicitly tested for normality. One reason for this is that there is no universally accepted threshold for deciding whether data is “normal enough” for parametric tests. Another reason is the power of normality tests varies depending on the sample size. In repeated dose administration studies, the number of animals in each group is often small (5–20). In such cases, normality tests may not provide meaningful results due to low statistical power, and the decision to use a parametric or nonparametric test often relies on other considerations, such as variance. It is a common practice to use equal-variance tests (for example Bartlett’s test, Levene’s test, etc.) to determine whether parametric or nonparametric methods should be used for analyzing data. In repeated dose administration toxicity studies for assessing normality the Shapiro-Wilk’s W (Shapiro-Wilk) test is recommended.