In the present study, the properties of the Lactiplantibacillus (Lpb.) plantarum WiKim0112 isolated from kimchi were evaluated by comparing its probiotic properties to those of Lpb. plantarum WCFS1 and KACC 11451 isolated from different sources. In both pH 2 and 3, media containing pepsin, Wikim0112, and WCFS1 showed higher cell viability than KACC11451. Viability of all Lpb. plantarum strains in a medium containing pancreatin and bile salt oxgall was significantly decreased compared to the control. WCFS1 showed the highest thermotolerance, followed by Wikim0112 and KACC11451. Wikim0112 showed a similar level of antibacterial activity to WCFS1 and exhibited an overall higher antibacterial activity than KACC11451 against six pathogens. All Lpb. plantatum strains showed high antioxidant activities in SOD, DPPH, and ABTS assays, especially Wikim0112 and WCFS1 exhibited a higher antioxidant activity than KACC11451. All Lpb. plantarum strains showed approximately 60–62% adhesion rates to Caco-2 cells. Moreover, in LPS-stimulated Caco-2 cells, all Lpb. plantarum strains significantly decreased the mRNA expression of pro-inflammatory cytokines (i.e., IL-1β, IL-6, and TNF-α); Wikim0112 significantly increased the mRNA expression of IL-4 and IFN-γ. Wikim0112 was resistant to streptomycin and vancomycin, whereas WCFS1 and KACC11451 were resistant to four (clindamycin, ciprofloxacin, tetracycline, and vancomycin) and three (ciprofloxacin, tetracycline, and vancomycin) antibiotics, respectively. These results, taken together, indicated that compared to Lpb. plantarum strains isolated from different sources, Wikim0112 showed desirable probiotic properties, suggesting its potential applications in the food and pharmaceutical industries.

Flutriafol (FTF) is a triazole fungicide that can cause liver toxicity through the ingestion of its residues in food and water. However, little is known about the liver toxicity of FTF, particularly nonalcoholic fatty liver disease (NAFLD) in humans. Therefore, the purpose of this study was to investigate whether FTF induces NAFLD in human liver cells and animal liver. HepG2 cells and Sprague Dawley (SD) rats were treated with FTF at doses of 0–640 µM for 24 h and 0–150 mg/kg bw/day for 28 days, respectively. FTF (80, 160, and 320 µM) treatment to cells induced lipid accumulation. FTF (80 and 160 µM)-treated cells had higher levels of cytochrome P450 enzymes and reactive oxygen species and increased mitochondrial membrane potential loss than the control. FTF also increased the mRNA levels of antioxidant enzymes through oxidative stress and nuclear factor erythroid 2-related factor 2 pathways in HepG2 cells. However, a higher level of FTF (320 µM) induced apoptosis. The treatment of SD rats with FTF (2.5–150 mg/kg bw/day) induced fatty infiltration in the liver by impairing liver metabolism and inducing apoptosis. Therefore, our data suggest that human exposure to FTF residues may be a risk factor for liver diseases, such as NAFLD.

Tebuconazole (TEB), a triazole fungicide, is frequently applied to agriculture for the increase of food production. Although TEB causes liver toxicity, its effects on cellular lipid accumulation are rarely investigated. Therefore, this study aimed to study the effects of TEB on lipid metabolism and accumulation in HepG2 cells. HepG2 cells were exposed to 0–320 µM TEB for 1–24 h. TEB (20–80 µM, 24 h)-treated cells showed lipid accumulation. Further, TEB (20–80 µM, 1–12 h) increased the nuclear translocation of peroxisome proliferator-activated receptors and the expression of lipid uptake and oxidation-related markers such as cluster of differentiation 36, fatty acid transport protein (FATP) 2, FATP5, and carnitine palmitoyltransferase 1. Oxidative stress levels in TEB-treated cells (20–80 µM, 24 h) were higher, compared to those in the control. TEB (20–80 µM, 24 h) also induced the loss of mitochondrial membrane potential and lower levels of microsomal triglyceride transfer protein in the cells. Thus, TEB can induce lipid accumulation by altering the expression of lipid-metabolizing molecules and can therefore impair lipid metabolism. Our data suggest that human exposure to TEB may be a risk factor for non-alcoholic fatty liver disease.