In plants, auxin/indoleacetic acid (Aux/IAA) proteins are transcriptional regulators that regulate developmental process and responses to phytohormones and stress treatments. However, the regulatory functions of the Vitis vinifera L. (grapevine) Aux/IAA transcription factor gene VvIAA18 have not been reported. In this study, the VvIAA18 gene was successfully cloned from grapevine. Subcellular localization analysis in onion epidermal cells indicated that VvIAA18 was localized to the nucleus. Expression analysis in yeast showed that the full length of VvIAA18 exhibited transcriptional activation. Salt tolerance in transgenic tobacco plants and Escherichia. coli was significantly enhanced by VvIAA18 overexpression. Real-time quantitative PCR analysis showed that overexpression of VvIAA18 up-regulated the salt stress-responsive genes, including pyrroline-5-carboxylate synthase (NtP5CS), late embryogenesis abundant protein (NtLEA5), superoxide dismutase (NtSOD), and peroxidase (NtPOD) genes, under salt stress. Enzymatic analyses found that the transgenic plants had higher SOD and POD activities under salt stress. Meanwhile, component analysis showed that the content of proline in transgenic plants increased significantly, while the content of hydrogen peroxide (H2O2) and malondialdehyde (MDA) decreased significantly. Based on the above results, the VvIAA18 gene is related to improving the salt tolerance of transgenic tobacco plants. The VvIAA18 gene has the potential to be applied to enhance plant tolerance to abiotic stress.

Cadmium (Cd) is a type of noxious heavy metal that is distributed widely. It can severely injure the hepatocytes and cause liver dysfunction by inducing oxidative stress and mitochondrial damage. We evaluated the protective effects of α-lipoic acid (α-LA) or chlorogenic acid (CGA) and their combination on counteracting cadmium toxicity in vivo in three-yellow chickens. For three months, CdCl2 (50 mg/L) was administrated through their drinking water, α-LA (400 mg/kg) was added to feed and CGA (45 mg/kg) was employed by gavage. The administration of Cd led to variations in growth performance, biochemical markers (of the liver, kidney and heart), hematological parameters, liver histopathology (which suggested hepatic injury) and ultrastructure of hepatocytes. Some antioxidant enzymes and oxidative stress parameters showed significant differences in the Cd-exposure group when compared with the control group. The groups treated with Cd and administrated α-LA or CGA showed significant amelioration with inhibited mitochondrial pathway-induced apoptosis. Combining both drugs was the most effective in reducing Cd toxicity in the liver. In summary, the results demonstrated that α-LA and CGA may be beneficial in alleviating oxidative stress induced by oxygen free radicals and tissue injury resulting from Cd-triggered hepatotoxicity.

Beauvericin (BEA), a food-borne mycotoxin metabolite derived from the fungus Beauveria Bassiana, is proven to exhibit high hepatotoxicity. However, the molecular mechanism underlying BEA-induced liver damage is not fully understood. Herein, the effect of Nrf2 nuclear translocation-induced by BEA in hepatocytes was investigated. CCK8 solution was used to determine the appropriate concentrations of BEA (0, 1, 1.5 and 2 μmol/L), and BRL3A cells were then exposed to different concentrations of BEA for 12 h. Our results reveal that BEA exposure is associated with high cytotoxicity, lowered cell viability, damaged cellular morphology, and increased apoptosis rate. BEA could lead to oxidative damage through the overproduction of ROS and unbalanced redox, trigger the activation of Nrf2 signaling pathway and Nrf2 nuclear translocation for transcriptional activation of downstream antioxidative genes. Additionally, BEA treatment upregulated the expression of autophagy-related proteins (LC3, p62, Beclin1, and ATG5) indicating a correlation between Nrf2 activation and autophagy, which warrants further studies. Furthermore, ML385, an Nrf2 inhibitor, partially ameliorated BEA-induced cell injury while CDDO, an Nrf2 activator, aggravated liver damage. The present study emphasizes the role of Nrf2 nuclear translocation in BEA-induced oxidative stress associated with the hepatotoxic nature of BEA.