Composite with a high specific surface area of 224.62 m2 g-1 was prepared by adding urea as a nitrogen source to hazelnut shell biochar (HSB). Nitrogen doping significantly enhanced the ability of biochar for Cr(VI) elimination, achieving twice the removal efficiency of unmodified biochar. The impacts of varying the pH and initial concentrations on Cr(VI) removal by urea-modified biochar (N-HSB) were investigated. The Cr(VI) removal by N-HSB was better described by intra particle diffusion model and pseudo-second order kinetic model under optimal conditions. Furthermore, XPS, FTIR, SEM, and BET analyses were used to verify the pivotal roles of oxygen- and nitrogen-containing functional groups. Electrostatic attraction, redox reaction, and complexation constituted the principal mechanisms facilitating Cr(VI) elimination by N-HSB. This study demonstrated that the modification of biochar with urea as a nitrogen source represented a promising strategy for enhancing the removal capacity of biochar for Cr(VI) in aqueous environments.

Hexavalent chromium (Cr(VI)) is a common pollutant in the marine environment, which impairs immunity and causes reproductive and heredity disorders in organisms. To clarify the immunotoxic effects of Cr (VI) on the marine worm Urechis unicinctus, we analyzed tissue damage and immune dysfunction caused by Cr (VI) in this organism at histopathologic, zymologic, apoptotic and molecular levels. The results indicated that the bioaccumulation of Cr (VI) bioaccumulation levels in coelomocytes was significantly higher than in the intestines and muscles. Pathological observation showed that Cr (VI) caused damage to the respiratory intestine, stomach and midgut. Cr (VI) also increased the replication of goblet cells and a reduction in the replication of epithelial cells. Meanwhile, Cr (VI) induced apoptosis of intestinal cells and coelomocytes, accompanied by an increase in the expression of Caspase-3, COX-2, and MyD88 in the intestine and coelomocytes. At the same time, Cr (VI) significantly affected the activities of antioxidant enzymes such as SOD, ACP, CAT, CAT, and GST, and increased H2O2 and MDA contents in U. unicinctus. Moreover, Cr (VI) exposure also up-regulated the transcription of hsc70, mt and jnk genes but decreased that of sod in the intestines. In contrast, Cr (VI) down-regulated the expression of sod, hsc70, mt, and jnk genes in coelomocytes. Collectively, Cr (VI) bioaccumulated in U. unicinctus cells and tissues, causing several histopathological changes, oxidative stress, and apoptosis of several cells in the organism, resulting in intestinal and coelomocyte damage and immune dysfunctioning.

Hexavalent chromium (Cr(VI)) exposure has been linked with gastrointestinal toxicity, whereas the molecular pathways and key targets remain elusive. Computational toxicology analysis predicted the correlation between protein phosphatase 2A (PP2A) and genes regarding Cr(VI)-induced intestinal injury. Here, we generated a mouse model with intestinal epithelium-specific knock-out of Ppp2r1a (encoding PP2A Aα subunit) to investigate the mechanisms underlying Cr(VI)-induced small intestinal toxicity. Heterozygous mice (HE) and matched wild-type (WT) littermates were administrated with Cr(VI) at 0, 5, 20, 80 mg/L for 28 successive days. Cr(VI) treatment led to crypt hyperplasia, epithelial cell apoptosis, and intestinal barrier dysfunction, accompanied by the decline of goblet cell counts and Occludin expression in WT mice. Notably, these effects were aggravated in HE mice, indicating that PP2A Aα deficiency conferred mice with susceptibility to Cr(VI)-induced intestinal injury. Integrated data analysis and biological experiments revealed Cr(VI) exposure could decrease YAP1 phosphorylation at Ser127 but increase protein expression and activity, together with elevated TAZ protein driving epithelial crypt cells proliferation following damage, suggesting the involvement of Hippo/YAP1 signaling pathway in Cr(VI)-induced intestinal toxicity. Nevertheless, the enhanced phosphorylation of YAP1 in HE mice resulted in proliferation/repair defects in intestinal epithelium, thereby exacerbating Cr(VI)-induced gut barrier dysfunction. Notably, by molecular docking and further studies, we identified Urolithin A, a microbial metabolite, attenuated Cr(VI)-induced disruption of intestinal barrier function, partly by modulating YAP1 expression and activity. Our findings reveal the novel molecular pathways participated in Cr(VI)-caused small intestinal injury and urolithin A could potentially protect against environmental hazards-induced intestinal diseases.

Low molecular weight organic acids (LMWOA) are commonly present in natural water and play a pivotal role in the reduction of Cr(VI). In frozen solutions, the efficiency of Cr(VI) reduction is significantly enhanced due to the freezing concentration effect. However, this facilitation is found to be contingent upon the functional groups of LMWOA in this study. To be specific, LMWOA and Cr(VI) can form five-membered ring complexes, which greatly enhance electron transfer efficiency through Ligand-to-Metal Charge Transfer (LMCT). DFT calculations indicate that oxygen-containing groups located on carbon atoms at α positions play a crucial role in forming these complexes, ultimately determining the kinetics of Cr(VI) reduction. Moreover, freezing not only increases proton concentrations but also reduces free water molecule content in the liquid-like layer (LLL), thereby affecting LMWOA species through regulation of protonation and hydrolysis, and subsequently impacting reaction mechanisms. The stoichiometric ratios between LMWOA and Cr(VI) exceed theoretical values due to complexation with Cr(III). The reduction of Cr(VI) by LMWOA in frozen solutions is inhibited by soil solution, while the degree of inhibition varies among different types of LMWOA.

Hexavalent chromium (Cr(VI)) causes testicular damage and reduces testosterone secretion. Testosterone synthesis relies on cholesterol as a raw material, and its availability can be affected by lipophagy. However, the role of lipophagy in Cr(VI)-induced testicular damage and reduced testosterone secretion remains unclear. In this study, we investigated the effect of Cr(VI) on lipid metabolism and lipophagy in the testes of ICR mice. Forty mice were randomly divided into four groups and exposed to different doses of Cr(VI) (0, 75, 100, 125mg/kg) for thirty days. Cr(VI) increased the rate of sperm abnormalities, decreased testosterone level, and decreased the levels of testosterone synthesis-related proteins, namely steroidogenic acute regulatory (StAR) and 3β-hydroxysteroid dehydrogenase (3β-HSD) proteins. Through metabolomic analysis, Oil Red O staining, and biochemical indicator (triglyceride and total cholesterol) analysis, Cr(VI) was found to disrupt testicular lipid metabolism. Further investigation revealed that Cr(VI) inhibited the AMP-activated protein kinase (AMPK)/sterol regulatory element-binding protein 1 (SREBP1) pathway, elevated levels of the autophagy-related proteins microtubule-associated protein 1 light chain 3B (LC3B) and sequestosome 1 (SQSTM1)/P62 and lipophagy-related proteins Rab7 and Rab10, while increasing colocalization of LC3B and Perilipin2. These findings suggest that Cr(VI) exposure leads to abnormal lipid metabolism in the testes by suppressing the AMPK/SREBP1 pathway and disrupting lipophagy, ultimately reducing testosterone level and inducing testicular damage.

Hexavalent chromium [Cr(VI)] is a highly hazardous heavy metal with multiple toxic effects. Occupational studies indicate that its accumulation in humans can lead to liver damage. However, the exact mechanism underlying Cr(VI)-induced hepatotoxicity remains unknown. In this study, we explored the role of CTH/H2S/Drp1 pathway in Cr(VI)-induced oxidative stress, mitochondrial dysfunction, apoptosis, and liver injury. Our data showed that Cr(VI) triggered apoptosis, accompanied by H2S reduction, reactive oxygen species (ROS) accumulation, and mitochondrial dysfunction in both AML12 cells and mouse livers. Moreover, Cr(VI) reduced cystathionine γ-lyase (CTH) and dynamin related protein 1 (Drp1) S-sulfhydration levels, and elevated Drp1 phosphorylation levels at Serine 616, which promoted Drp1 mitochondrial translocation and Drp1-voltage-dependent anion channel 1 (VDAC1) interactions, ultimately leading to mitochondria-dependent apoptosis. Elevated hydrogen sulfide (H2S) levels eliminated Drp1 phosphorylation at Serine 616 by increasing Drp1 S-sulfhydration, thereby preventing Cr(VI)-induced Drp1-VDAC1 interaction and hepatotoxicity. These findings indicated that Cr(VI) induced mitochondrial apoptosis and hepatotoxicity by inhibiting CTH/H2S/Drp1 pathway and that targeting either CTH/H2S pathway or Drp1 S-sulfhydration could serve as a potential therapy for Cr(VI)-induced liver injury.

The occurrence of chromium picolinate (Cr(pic)3) in environment has attracted raising concerns on its fate and the associated risks. Herein, the photoinduced oxidation of Cr(pic)3 in the presence of ferric ions (Fe(III)) under simulated sunlight and natural solar light irradiation were investigated. Cr(pic)3 was stable under dark or without Fe(III). 87.9 % of Cr(pic)3 (C0 = 1.0 μM) was degraded in the presence of 50 μM Fe(III) after 90 min simulated sunlight irradiation at initial pH of 4.0. •OH was the main cause for Cr(pic)3 oxidation, it attacked the chromium center to generate hexavalent chromium (Cr(VI)) and picolinic acid (k = 5.9 ×108 M-1·s-1). Picolinic acid could be further oxidized to NH4+ and small organics. Relative higher Fe(III) content (25 - 75 μM) and Cr(pic)3 concentration (0.5 - 2.0 μM) promoted both of Cr(pic)3 degradation and Cr(VI) accumulation. While, the degradation of Cr(pic)3 decreased with pH at the range of 3.0 - 8.0, more Cr(VI) was accumulated at pH 5.0 and 6.0. The co-existence of inorganic ions and dissolved organic matter (DOM) in river water inhibited Cr(pic)3 oxidation by scavenging the •OH formed and shielding the light. 8.0 - 16.7 μg/L of Cr(VI) was accumulated after 9.0 h simulated sunlight irradiation of Cr(pic)3 in river water matrix ([Fe(III)]0 = 50 - 100 μM). The generation of Cr(VI) under solar light was slower than that under simulated sunlight due to the weaker light intensity (43.2 - 85.0 mW/cm2 vs. 750 - 1300 mW/cm2). These results consistently suggest photoinduced oxidation of Cr(pic)3 in environment generates the toxic Cr(VI), which deserves significant attention.

Microbially induced carbonate precipitation (MICP) is a common biomineralization method, which is often used for remediation of heavy metal pollution such as hexavalent chromium (Cr(VI)) in recent years. Calcium sources are essential for the MICP process. This study investigated the potential of MICP technology for Cr(VI) remediation under the influence of three calcium sources (CaCl2, Ca(CH3COO)2, Ca(C6H11O7)2). The results indicated that CaCl2 was the most efficient in the mineralization of Cr(VI), and Ca(C6H11O7)2 could significantly promote Cr(VI) reduction. The addition of different calcium sources all promoted the urease activity of Sporosarcina saromensis W5, in which the CaCl2 group showed higher urease activity at the same Ca2+ concentration. Besides, with CaCl2, Ca(CH3COO)2 and Ca(C6H11O7)2 treatments, the final fraction of Cr species (Cr(VI), reduced Cr(III) and organic Cr(III)-complexes) were mainly converted to the carbonate-bound, cytoplasm and cell membrane state, respectively. Furthermore, the characterization results revealed that three calcium sources could co-precipitate with Cr species to produce Ca10Cr6O24(CO3), and calcite and vaterite were present in the CaCl2 and Ca(CH3COO)2 groups, while only calcite was present in the Ca(C6H11O7)2 group. Overall, this study contributes to the optimization of MICP-mediated remediation of heavy metal contaminated soil. CaCl2 was the more suitable calcium source than the other two for the application of MICP technology in the Cr(VI) reduction and mineralization.

Introduction: Hexavalent chromium [Cr (VI)] has been identified as a human carcinogen and environmental pollutant capable of affecting multiple systems in the human body. However, the specific mechanisms by which Cr (VI) affects the human nervous system remain unclear. Objective: Following confirmation of Cr (VI)\'s toxic effects on rat astrocytes, this study explores the metabolites and associated metabolic pathways of rat astrocytes under different doses of Cr (VI) exposure. Methods: Cell viability was assessed using CCK8 assays, intracellular reactive oxygen species (ROS) levels were measured using DCFH-DA fluorescent probes, intracellular 8-hydroxydeoxyguanosine (8-OHdG) content was determined by Elisa, mitochondrial membrane potential was observed using JC-1 probes, and key metabolites were identified through untargeted metabolomics analysis. Results: With increasing Cr (VI) doses, significant decreases in cell viability were observed in the 4, 8, and 16 mg/L dose groups (p < 0.05). Elevated levels of ROS and 8-OHdG, increased caspase-3 activity, and significant reductions in mitochondrial membrane potential were observed in the 2 and 4 mg/L dose groups (p < 0.05). Untargeted metabolomics analysis revealed Cr (VI)\'s impact on key metabolites such as sphingosine and methionine. Enrichment analysis of KEGG pathways highlighted the critical roles of sphingolipid metabolism and the methionine-cysteine cycle in the effects of Cr (VI) on rat astrocytes. Conclusion: Our study underscores the potential neuro-health risks associated with environmental and occupational exposure to Cr (VI) and provides new perspectives and directions for investigating neurotoxic mechanisms.

Mitochondrial Pyruvate Carrier 1 (MPC1) is localized on mitochondrial outer membrane to mediate the transport of pyruvate from cytosol to mitochondria. It is also well known to act as a tumor suppressor. Hexavalent chromium (Cr (VI)) contamination poses a global challenge due to its high toxicity and carcinogenesis. This research was intended to probe the potential mechanism of MPC1 in the effect of Cr (VI)-induced carcinogenesis. First, Cr (VI)-treatments decreased the expression of MPC1 in vitro and in vivo. Overexpression of MPC1 inhibited Cr (VI)-induced glycolysis and migration in A549 cells. Then, high mobility group A2 (HMGA2) protein strongly suppressed the transcription of MPC1 by binding to its promoter, and HMGA2/MPC1 axis played an important role in oxidative phosphorylation (OXPHOS), glycolysis and cell migration. Furthermore, endoplasmic reticulum (ER) stress made a great effect on the interaction between HMGA2 and MPC1. Finally, the mammalian target of the rapamycin (mTOR) was determined to mediate MPC1-regulated OXPHOS, aerobic glycolysis and cell migration. Collectively, our data revealed a novel HMGA2/MPC-1/mTOR signaling pathway to promote cell growth via facilitating the metabolism reprogramming from OXPHOS to aerobic glycolysis, which might be a potential therapy for cancers.