Atrazine (ATR), a widely used herbicide, poses significant environmental and health risks due to its high solubility and adsorption in soil. ATR exposure can lead to nephrotoxicity in humans and animals. Curcumin (Cur), an active compound in Curcuma species, is renowned for its antioxidant and anti-inflammatory properties, with potential to mitigate chronic disease risks. We hypothesized that the addition of Cur could alleviate renal impairment associated with ATR exposure and carried out experiments using mice as subjects. This study investigates whether Cur can attenuate ATR-induced nephrotoxicity in mice by modulating mitophagy and apoptotic pathways. Our findings illustrate that consumption with Cur attenuates nephrotoxicity induced by ATR, as evidenced by lowered serum concentrations of uric acid (UA), blood urea nitrogen (BUN), and creatinine (CRE), established biomarkers of renal injury. Moreover, Curcumin enhances renal antioxidant defense mechanisms in ATR-exposed mice, as indicated by elevated levels of total antioxidant capacity (T-AOC), catalase (CAT), and glutathione peroxidase (GSH-Px), alongside reduced levels of malondialdehyde (MDA). Histopathological and electron microscopy analyses further corroborate these findings, showing reduced organelle damage, particularly mitochondrial ridge breakage and vacuolization, and increased autophagic lysosomes. Cur further enhances PINK1/Parkin-mediated autophagy, as evidenced by elevated levels of PINK1, Parkin, LC3BII, and P62 compared to ATR-treated mice. Moreover, Cur mitigates the mitochondrial apoptotic pathway, indicated by the down-regulation of apoptosis-related genes (Cytochrome C (Cyto-C), Caspase3, Caspase9) and the proapoptotic marker (Bax), along with the up-regulation of the anti-apoptotic marker (Bcl-2) at both transcriptional and translational levels compared to ATR-treated mice. In summary, Cur demonstrates nephroprotective properties against ATR-induced injury through the enhancement of mitochondrial autophagy and display of antiapoptotic actions, underscoring its curative potency as a treatment for nephrotoxicity caused by ATR.

Cadmium (Cd) is one of the highly toxic heavy metals that restricts plant growth, affects crop yields, and triggers food crises. Dimethyl sulfoxide (DMSO) is frequently used solvent in biological studies, and its potential application in resistance to Cd toxicity in plants and animals has not been reported. Here, low concentrations of DMSO alone were demonstrated to increase the biomass of pak choi seedlings; more importantly, under Cd stress conditions, DMSO was shown to reduce Cd accumulation, and thereby alleviate Cd-induced damages. Specifically, DMSO could enhance plant defense mechanisms against Cd stress by strengthening the activities of endogenous reactive oxygen species (ROS)-scavenging enzymatic or non-enzymatic antioxidants, regulating the expression of key stress-responsive genes, as well as activating autophagy and apoptosis protection in root cells, thereby scavenging excessive ROS, restoring integration of cell membranes, and conferring tolerance to Cdinduced phytotoxicity. Our results showed that DMSO could play a vital role in mitigating Cd-induced oxidative damage by activating the protective mechanisms generated by the synergistic effects of both autophagy and antioxidants. These findings will help to formulate strategies to mitigate Cd contamination and to ensure the safety of cabbage production, an important vegetable source.

The application of uranium (U) in the nuclear energy and defense industry has driven U mining activities, leading to subsequent U contamination. Understanding the toxicity and detoxification mechanism of U in plants is crucial for enhancing the efficiency of phytoremediation efforts in U-contaminated soils. The present study investigated the toxicity of uranium (U) in radish and its impact on physiological and molecular responses. The application of U (5-25 mu M) for 3 days significantly inhibited the elongation of radish lateral roots, and the lateral root length decreased by 35.6%-60.7% compared with the control. Under U stress, radish root tip meristem cells suffered DNA damage, fortunately the cells remained viable. To repair damaged DNA, the expression of genes involved in DNA repair (e.g. RAD2, XPC, BLM) was up-regulated, and the expression of genes involved in cell cycle was down-regulated (e.g. CYCB, CDKB). Under U stress, the expression of respiratory burst oxidase homologs (RBOHs) genes in radish roots up-regulated, which caused ROS burst, and then enhanced autophagy by promoting the expression of autophagy related genes (ATGs). Simultaneously, the glutathione (GSH) content increased, and the gene expression levels and activities of antioxidant enzymes (e.g. catalase) were increased, which enhanced the antioxidant capacity of root cells. Moreover, ubiquitin-proteasome system (UPS) (e.g. E3 ligase genes NEDD4) was involved in the activation of DNA repair, GSH synthesis and autophagy. In summary, DNA repair, autophagy, and antioxidant systems were activated in radish roots, which promoted the survival of apical meristem cells under U stress.

Atrazine (ATR) is a widely used agricultural herbicide, and its accumulation in soil and water can cause various environmental health problems. ATR has neurotoxic effects on dopaminergic neurons, which can lead to a Parkinson's disease (PD)-like syndrome. Epigenetics regulates gene expression dynamically through DNA methylation, histone post-translational modification, microRNA (miRNA) interaction, and RNA methylation. MicroRNA (miRNA), representing one of the primary epigenetic mechanisms responsible for regulating gene expression, plays a crucial role in maintaining normal cellular function, while dysregulation of miRNA expression has been observed in PD. This study aims to investigate the regulatory mechanisms of miRNA in ATR exposure. The results show that ATR-exposure significantly upregulates the expression level of miR-217-5p. Both miR-217-5p overexpression and ATR exposure is able to trigger the autophagy process and apoptosis. Conversely, inhibiting the expression of miR-217-5p can reverse the levels of ATR-induced autophagy and apoptosis. Moreover, ATR causes damage to dopaminergic neurons, as indicated by the altered expression of tyrosine hydroxylase and alpha-synuclein. Taken together, these results suggest that ATR-induced autophagy can accelerate the progression of neurodegenerative diseases and that miR-217-5p is probably an important target involved in ATR-induced dopaminergic damage, shedding important light on the development of a novel strategy for treating neurodegenerative diseases.