Toxic Effects Of Cr Research Articles

Cr(VI) induces ferroptosis in DF-1 cells by simultaneously perturbing iron homeostasis of ferritinophagy and mitophagy

Hexavalent chromium [Cr(VI)] is an environmental pollutant known for its strong oxidizing and carcinogenic effects. However, its potential to induce ferroptosis in poultry remains poorly understood. This study aims to investigate the induction of ferroptosis by Cr(VI) in DF-1 cells and elucidate the underlying mechanisms. DF-1 cells exposed to Cr(VI) showed increased lipid reactive oxygen species and changes in ferroptosis marker genes (decreased expression of GPX4 and increased expression of COX2). Notably, the addition of the ferroptosis-specific inhibitor ferrostatin-1 (Fer-1) can reverse this effect. During the cell death process, Cr(VI) induced ferritinophagy, disrupting iron homeostasis and releasing labile iron ions. We predicted by docking that these iron ions would bind to mitochondrial membrane proteins through virtual docking. This binding was validated through colocalization analysis. In addition, Cr(VI) caused mitophagy, which releases additional ferrous ions. Therefore, Cr(VI) can induce the simultaneous release of ferrous ions through these pathways, thereby exacerbating lipid peroxidation and ultimately triggering ferroptosis in DF-1 cells. This study demonstrates that Cr(VI) can induce ferroptosis in DF-1 cells by disrupting intracellular iron homeostasis and providing valuable insights into the toxic effects of Cr(VI) in poultry and potentially other organisms.

Toxic effects of Cr, Cu, Se, Cd, Hg and Pb ions on the environment and human health: a review

Toxic effects of Cr, Cu, Se, Cd, Hg and Pb ions on the environment and human health: a review

YTHDF2 controls hexavalent chromium-induced mitophagy through modulating Hif1α and Bnip3 decay via the m6A/mRNA pathway in spermatogonial stem cells/progenitors

Spermatogonial stem cells (SSCs) are the basis of spermatogenesis, and SSC homeostasis is essential for lifelong male fertility. Currently, environmental pollution remains one of the factors affecting human reproductive health. Chromium is a prevalent metal element, and excessive exposure to hexavalent chromium (Cr (VI)) can cause male reproductive disorders. Nevertheless, the toxic effects of Cr (VI) on SSCs and the underlying mechanisms remain incompletely understood. Here, we showed that Cr (VI) exposure triggered mitophagy in mouse SSCs/progenitors in a time-dependent manner. Concurrently, Cr (VI) treatment caused reactive oxygen species (ROS) accumulation and activated the HIF1α-mediated BNIP3 expression to trigger mitophagy. In addition, Cr (VI) exposure significantly decreased the level of m6A modification. Further, we identified that YTHDF2 regulated the stability of Bnip3 and Hif1α mRNAs in an m6A-dependent manner, which was involved in Cr (VI)-induced mitophagy. Collectively, our study not only expands the mechanisms for Cr (VI)-caused male reproductive toxicity, but also provides pharmacological targets for prevention and treatment of Cr (VI)-induced male fertility impairment.

Effects of microplastic combined with Cr(III) on apoptosis and energy pathway of coral endosymbiont.

The combined effect of polyethylene (PE) microplastics and chromium (Cr(III)) on the scleractinian coral Acropora pruinosa (A. pruinosa) was investigated. The endpoints analysed in this study included the endosymbiont density, the chlorophyll a + c content, and the activity of enzymes involved in apoptosis (caspase-1, caspase-3), glycolysis (lactate dehydrogenase, LDH), the pentose phosphate pathway (glucose-6-phosphate dehydrogenase, G6PDH) and electron transfer coenzyme (nicotinamide adenine dinucleotide, NAD+/NADH). During the 7-day exposure to PE and Cr(III) stress, the endosymbiont density and chlorophyll content decreased gradually. The caspase-1 and caspase-3 activities increased in the high-concentration Cr(III) exposure group. Furthermore, the LDH and G6PDH activities decreased significantly, and the NAD+/NADH was decreased significantly. In summary, the results showed that PE and Cr(III) stress inhibited the endosymbiont energy metabolism enzymes and further led to endosymbiont apoptosis in coral. In addition, under exposure to the combination of stressors, when the concentration of Cr(III) remained at 1 × 10-2mg/L, the toxic effects of heavy metals on the endosymbiont were temporarily relieved with elevated PE concentrations. In contrast, when coral polyps were exposed to 5mg/L PE and increasing Cr(III) concentrations, their metabolic activities were seriously disturbed, which increased the burden of energy consumption. In the short term, the toxic effect of Cr(III) was more obvious than that of PE because Cr(III) exposure leads to endosymbiont apoptosis and irreversible damage. This is the first study to provide insights into the combined effect of microplastic and Cr(III) stress on the apoptosis and energy pathways of coral endosymbionts. This study suggested that microplastics combined with Cr(III) are an important factor affecting the apoptosis and energy metabolism of endosymbionts, accelerating the collapse of the balance between the coral host and symbiotic endosymbiont.

Efficacy of metallic nanoparticles in attenuating the accumulation and toxicity of chromium in plants: Current knowledge and future perspectives

Nanoparticles have emerged as cutting-edge technology for the improvement of crops yield and safe cultivation of agricultural plants, especially in peripheral areas impaired with toxic heavy metals including chromium (Cr). The uncontrolled release of Cr mainly from anthropogenic factors is substantially polluting the surrounding environment, thereby extensively accumulated in soil-plant system. The excessive Cr-accretion in plant tissues disturbed the morph-physiological, biochemical, cellular, metabolic and molecular processes, and impaired the plants functionality. Therefore, it is obligatory to restrict the accumulation and toxic effects of Cr in plant organs. Recent studies on metallic nanoparticles (MNPs) such as iron oxide, silicon dioxide, copper oxide and zinc oxide have approved their efficacy as potent pool to curb the Cr-induced phytotoxicities and improved the plant tolerance. MNPs attenuated the bioaccumulation and phytotoxicity of Cr by utilizing key mechanisms such as improved photosynthetic machinery, regulation of cellular metabolites, greater chelation capacity to bind with Cr, release of corresponding metallic ions, upsurge in the uptake of essential nutrients, activation of antioxidants (enzymatic and non-enzymatic), reduction in oxidative stress, and cellular injuries, thus improvement in plant growth performances. We have briefly discussed the current knowledge and research gaps in existing literature along with possible recommendations for future research. Overall, Cr-detoxification by MNPs may depends upon the target plant species, Cr speciation, plant growth stages (seedling, vegetative and ripening etc.), treatment methods (foliar spray, seed priming and nutrient solution etc.), type, size, dose and coating of applied MNPs, and conditions (hydroponic and soil environment etc.). This review would help plant scientists to develop MNPs based strategies such as nano-fertilizers to alleviate the Cr-accumulation and its toxic impacts. This may leads to safe and healthy food production. The review outcomes can provide new horizons for research in the applications of MNPs for the sustainable agriculture.

Chromium [Cr(VI)] Exposure Causes Cytotoxicity of Human Bronchial Epithelial Cells (16-HBE) and Proteomic Alterations.

Hexavalent chromium [Cr(VI)] is a common industrial pollutant, and exposure may cause toxic effects in multiple organ systems and carcinogenesis, including lung cancer. However, the toxic effect of Cr(VI) on the respiratory system is poorly understood. In the present study, it was demonstrated that Cr(VI) exposure significantly decreased the viability of human bronchial epithelial cells (16-HBE) in a dose-dependent manner. Flow cytometry demonstrated that Cr(VI) enhanced the transition of 16-HBE cells from G1 to S phase and arrested S-phase progression. Reverse transcription-quantitative polymerase chain reaction analysis revealed a significant alteration in the expression of apoptosis-associated genes in Cr(VI)-treated 16-HBE cells. In addition, using two-dimensional fluorescence differential gel electrophoresis with mass spectrometry, 15 differentially expressed proteins (1 upregulated and 14 downregulated) were identified in 16-HBE cells with Cr(VI) treatment compared with controls. Functional classification revealed that these differentially expressed proteins were involved in apoptosis, cytoskeletal structure, and energy metabolism. In conclusion, these data suggested that Cr(VI) caused toxic effects in bronchial epithelial cells and the mechanisms may involve the abnormal expression of apoptosis-associated proteins, cytoskeletal proteins, and energy metabolism-associated proteins.

Regulation of Cr(VI)-Induced Premature Senescence in L02 Hepatocytes by ROS-Ca2+-NF-κB Signaling.

Stress-induced premature senescence may be involved in the pathogeneses of acute liver injury. Hexavalent chromium [Cr(VI)], a common environmental pollutant related to liver injury, likely leads to premature senescence in L02 hepatocytes. However, the underlying mechanisms regarding hepatocyte premature senility in Cr(VI) exposure remain poorly understood. In this study, we found that chronic exposure of L02 hepatocytes to Cr(VI) led to premature senescence characterized by increased β-galactosidase activity, senescence-associated heterochromatin foci, G1 phase arrest, and decreased cell proliferation. Additionally, Cr(VI)-induced senescent L02 hepatocytes showed upregulated inflammation-related factors, such as IL-6 and fibroblast growth factor 23 (FGF23), which also exhibited reactive oxygen species (ROS) accumulation derived from mitochondria accompanied with increased concentration of intracellular calcium ions (Ca2+) and activity of nuclear factor kappa B (NF-κB). Of note is that ROS inhibition by N-acetyl-Lcysteine pretreatment not only alleviated Cr(VI)-induced premature senescence but also reduced the elevated intracellular Ca2+, activated NF-κB, and secretion of IL-6/FGF23. Intriguingly, the toxic effect of Cr(VI) upon premature senescence of L02 hepatocytes and increased levels of IL-6/FGF23 could be partially reversed by the intracellular Ca2+ chelator BAPTA-AM pretreatment. Furthermore, by utilizing the NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC), we confirmed that NF-κB mediated IL-6/FGF23 to regulate the Cr(VI)-induced L02 hepatocyte premature senescence, whilst the concentration of intracellular Ca2+ was not influenced by PDTC. To the best of our knowledge, our data reports for the first time the role of ROS-Ca2+-NF-κB signaling pathway in Cr(VI)-induced premature senescence. Our results collectively shed light on further exploration of innovative intervention strategies and treatment targeting Cr(VI)-induced chronic liver damage related to premature senescence.

Hexavalent chromium inhibits the formation of neutrophil extracellular traps and promotes the apoptosis of neutrophils via AMPK signaling pathway

As the most common heavy metal pollutant, hexavalent chromium [Cr(VI)] has caused serious environmental pollution and health damage. Although the toxic effect of Cr(VI) has been widely studied, and oxidative stress has been confirmed to be the main mechanism of its cytotoxicity, the toxicity of Cr(VI) to human immune system remains to be elucidated. Neutrophil extracellular traps (NETs) participate in the innate immune response, and the release of NETs is considered to be the most important part of the extracellular killing mechanism. We demonstrated in this study that Cr(VI) inhibited the formation of NETs in rat peripheral blood and induced neutrophils apoptosis by inhibiting the AMP-activated protein kinase (AMPK) signaling pathway. Cr(VI)-induced inhibition of NETs was accompanied by down-regulated myeloperoxidase (MPO)/Histones-3 (H3) protein expressions and decreased NETs-associated intracellular and extracellular DNA levels in the neutrophils. Metformin (Met), as an AMPK activator, triggered autophagy and thus alleviated the inhibitory effect of Cr(VI) on NETs. At the same time, Met can reduce the intracellular reactive oxygen species (ROS) level by activating the AMPK/nuclear factor erythroid-2 related factor 2 (Nrf2) signaling pathway, thus alleviating Cr(VI)-induced neutrophils apoptosis. In conclusion, this study elucidated the mechanism of Cr(VI)-induced neutrophils toxicity and the role of AMPK as a key regulatory signal, which could provide valuable experimental basis for the prevention and treatment of related diseases in Cr(VI)-exposed populations.

Melatonin Attenuates Chromium (VI)-Induced Spermatogonial Stem Cell/Progenitor Mitophagy by Restoration of METTL3-Mediated RNA N6-Methyladenosine Modification.

Spermatogonial stem cells (SSCs) are the basis of spermatogenesis, and any damage to SSCs may result in spermatogenic disorder and male infertility. Chromium (Cr) (VI) is a proven toxin, mutagen, and carcinogen, perpetually detrimental to environmental organisms due to its intricate and enduring detoxification process in vivo. Despite this, the deleterious effects of Cr (VI) on SSCs and the underlying mechanisms remain poorly understood. In this study, we identified that Cr (VI) impaired male reproductive system in mouse testes and induced mitochondrial dynamic imbalance and mitophagy in SSCs/progenitors. Cr (VI) also downregulated the RNA N6-methyladenosine (m6A) modification levels in mitochondrial dynamic balance and mitophagy genes in SSCs/progenitors. Inspiringly, the toxic effects of Cr (VI) could be relieved by melatonin pretreatment. Melatonin alleviated Cr (VI)-induced damage to male reproductive system and autophagy in mouse testes. Melatonin also attenuated Cr (VI)-induced cell viability loss and reactive oxygen species (ROS) generation, as well as mitochondrial dynamic disorders and mitophagy in SSCs/progenitors. The protective roles of melatonin against Cr (VI)-induced mitophagy were exerted by restoration of METTL3-mediated RNA m6A modification and activation of mitochondrial fusion proteins MFN2 and OPA1, as well as inhibition of the mitophagy BNIP3/NIX receptor pathway. Thus, our study provides novel insights into the molecular mechanisms for RNA m6A modification underlying the gene regulatory network responsible for mitochondrial dynamic balance, and also lays new experimental groundwork for treatment of Cr (VI)-induced damage to male fertility.

Azotobacter vinelandii helps to combat chromium stress in rice by maintaining antioxidant machinery.

Chromium (Cr) causes toxic effects in plants by generating reactive oxygen species (ROS) which create oxidative environment. Azotobacter vinelandii helps in growth and development of many crops; however, its role in Cr stress tolerance in rice has not been explored. Here, we report the new function of Azotobacter vinelandii strain SRI Az3 (Accession number JQ796077) in providing Cr stress tolerance in Oryza sativa (var. IR64). The efficiency of the strain was checked under different concentrations (50, 100, 150, 200 and 250µM) of Cr stress and it was observed that it provides stress tolerance to rice plant up to 200µM concentration. Different agronomic growth parameters were found to be better in this strain of Azotobacter vinelandii-inoculated rice plants as compared to un-inoculated one. The agronomic growth and photosynthetic characteristics such as net photosynthetic rate (PN), stomatal conductance (gs), intercellular CO2 (Ci) were also found to be significantly increased with increasing concentration of Azotobacter vinelandii inoculation. The activities of antioxidant enzymes were significantly higher (35%) in rice plants inoculated with Azotobacter vinelandii as compared with un-inoculated rice plant. All these positive effects of Azotobacter vinelandii help rice to survive from the toxic effect of Cr.

COMPLEX EFFECT OF CHROME AND SALINATION ON NITROGEN EXCHANGE IN PUMPKIN PLANTS

A specific character of physiological-biochemical stress responses of pumpkin plants to toxic effect of cadmium under conditions of salinity in the course of their long-term cross-adaptation was investigated. Cr and NaCl were added either alone or in combination in Knop solution along with non-treated controls. In 7- and 14- day plants, all the physiological processes studied (shoot and root growth, bioaccumulation of fresh and dry biomass by them and nitrogen-protein metabolism in different plant organs) were found to be more sensitive to inhibitory action of Cr excess than to NaCl effect. However, in 21-day plants, especially in their roots, a some activation of growth and biosynthetic processes was observed in the presence of combined Cr and NaCl treatments than at their lone application. All this indicates that an adaptation of plants to salinity is accompanied by a some reduction in toxic effect of Cr on growth and metabolism of plants

Ліпідний склад плазми крові щурів за дії етилтіосульфанілату і хром (VI)-індукованої токсичності

Ethylthiosulfanylate (ETS) is synthetic organosulfur compound and belongs to the class of thiosulfonates, which are the structural analogues of natural BACs of plant origin. Thiosulfonates and ETS in particular affect the regulation of pro/antioxidant status, lipid and protein metabolism in the tissues of laboratory rats. Cr(VI) compounds are characterized by potent prooxidant properties and high toxicity for cells of living organisms. The toxic effect of Cr(VI)-induced oxidative stress is accompanied by lipid metabolism disorders and the correction methods have not been sufficiently studied. The aim of our study was to investigate the effect of ETS on some indicators of lipid metabolism in blood plasma of rats under the action of K2Cr2O7-induced toxicity. Animals were divided into 7 groups. Animals of group I injected daily intraperitoneally with 150 μl of physiological solution for 7 days. Experimental groups III and IV were administered daily intraperitoneally with K2Cr2O7 in a dose of 2.5 mg Cr(VI)/kg body weight, for 7 (group III) and 14 days (group IV). Rats of group II received intragastric injection of 1000 μl of oil daily for 14 days, than animals were injected daily intraperitoneally with 150 μl of physiological solution for 7 days. Experimental group V was intragastrically injected with ETS oily solution at a rate of 100 mg/kg of body weight daily for 14 days, than animals were injected intraperitoneally 150 μl of physiological solution daily for 7 days. Animals of groups VI and VII were intragastrically administered with ETS oily solution at a rate of 100 mg/kg of body weight daily for 14 days, than animals were injected intraperitoneally daily K2Cr2O7 in a dose of 2.5 mg Cr(VI)/kg body weight, for 7 (group VI) and 14 days (group VII). Rats were decapitated under thiopental anesthesia, after which blood was taken and divided into erythrocytes and plasma. The Cr(VI) action for 7 (group III) and 14 days (group IV) led to an increase in the content of total lipids and triglycerides in the blood plasma of rats, but the percentage of nonesterified cholesterol decreased. ETS partially compensates the Cr(VI)-induced toxicity by reducing the intensity of total lipids (groups VI, VII) and triglycerides (group VI) accumulation.

Effect of Interaction between 17β-Estradiol, 2-Methoxyestradiol and 16α-Hydroxyestrone with Chromium (VI) on Ovary Cancer Line SKOV-3: Preliminary Study.

Ovarian cancer is the leading cause of death from gynecologic malignancies. Some estrogens, as well as xenoestrogens, such as chromium (VI) (Cr(VI)), are indicated as important pathogenic agents. The objective of this study was to evaluate the role of estradiol and some its metabolites upon exposure to the metalloestrogen Cr(VI) in an in vitro model. The changes in cell viability of malignant ovarian cancer cells (SKOV-3 resistant to cisplatin) exposed to 17β-estradiol (E2) and its two metabolites, 2-methoxyestradiol (2-MeOE2) and 16α-hydroxyestrone (16α-OHE1), upon exposure to potassium chromate (VI) and its interactions were examined. The single and mixed models of action, during short and long times of incubation with estrogens, were applied. The different effects (synergism and antagonism) of estrogens on cell viability in the presence of Cr(VI) was observed. E2 and 16α-OHE1 caused a synergistic effect after exposure to Cr(VI). 2-MeOE2 showed an antagonistic effect on Cr(VI). The examined estrogens could be ranked according to the most protective effect or least toxicity in the order: 2-MeOE2 > E2 > 16α-OHE1. Early pre-incubation (24 h or 7 days) of cells with estrogens caused mostly an antagonistic effect—protective against the toxic action of Cr(VI). The beneficial action of estrogens on the toxic effect of Cr(VI), in the context of the risk of ovarian cancer, seems to be important and further studies are needed.

Exogenous application of hydrogen sulfide reduces chromium toxicity in maize seedlings by suppressing NADPH oxidase activities and methylglyoxal accumulation

Chromium (Cr) represents an important source of metallic stress in plants. Working with maize (Zea mays) seedlings, we characterize the suppressive effects of exogenously applied NaHS (a hydrogen sulfide; [H2S] donor) on the toxic effects of Cr (VI). Heavy metal treatment reduced radicle and epicotyl lengths and fresh weights in seedlings at 6 and 9 days following germination. The negative Cr (200 μM) effect was countered by application with NaHS (500 μM) but this countering was reduced with the co-application of the H2S generation inhibitor hydroxylamine (HA) or the H2S scavenger hypotaurine (HT). The Cr-elicited H2O2 production was suppressed by NaHS and also by an inhibitor of the reactive oxygen species (ROS) generating NADPH oxidase (NOX). These effects were correlated with relative changes in carbomyl (-CO) and thiol (-SH) groups. Nitric oxide (NO) production increased by NaHS application with associated increase in S-nitrosoglutathione (GSNO) level, but low S-nitrosoglutathione reductase (GSNOR) activities indicating an elevated S-nitrosylation. Assessment of the role of the ascorbate-glutathione antioxidant cycle indicated that whilst ascorbate played at a best minor role, glutathione was more prominent. Methylglyoxal (MG) production was increased by Cr but reduced by NaHS through a mechanism which could be based on glutathione-S-transferase (GST) detoxification. Taken together data suggest that H2S acts to counter Cr effect in maize by NOX suppression, mostly likely by the well-characterised S-nitrosylation mechanism, as well as a reduction of MG accumulation.

Chromium Bioaccumulation and Its Impacts on Plants: An Overview.

Chromium (Cr) is an element naturally occurring in rocky soils and volcanic dust. It has been classified as a carcinogen agent according to the International Agency for Research on Cancer. Therefore, this metal needs an accurate understanding and thorough investigation in soil–plant systems. Due to its high solubility, Cr (VI) is regarded as a hazardous ion, which contaminates groundwater and can be transferred through the food chain. Cr also negatively impacts the growth of plants by impairing their essential metabolic processes. The toxic effects of Cr are correlated with the generation of reactive oxygen species (ROS), which cause oxidative stress in plants. The current review summarizes the understanding of Cr toxicity in plants via discussing the possible mechanisms involved in its uptake, translocation and sub-cellular distribution, along with its interference with the other plant metabolic processes such as chlorophyll biosynthesis, photosynthesis and plant defensive system.

The acute toxicity effects of hexavalent chromium in antioxidant system and gonad development to male clam Geloina coaxans

Hexavalent chromium (Cr(VI)) is a harmful environmental pollutant, which is widely distributed in the marine environment. However, the mechanisms underlying Cr-induced oxidative stress and reproductive toxicity in clams remain largely unknown. The objective of this study was to explore the acute toxic effects of Cr(VI) and estimate the applicability of male clam Geloina coaxans as a bioindicator in mangrove ecosystems. In this study, G. coaxans were exposed to 4.34, 8,69, 17.38 and 34.76 mg/L Cr(VI) for 24, 48 and 72 h. The activities of catalase (CAT), glutathione S-transferase (GST) and the content of malondialdehyde (MDA) were determined. The gene expression of CAT, GST, autophagy-related gene 5 (ATG5), cyclin B3 and spermatogenesis associated protein 4 (SAP4) were measured by RT-qPCR. Furthermore, histological alteration of the gonad and sperm was observed by light microscopy and transmission electron microscopy. The results showed that Cr(VI) exposure induced the accumulation of MDA and activities of enzymes. Cr(VI) exposure also inhibited the mRNA expression of ATG5, cyclin B3 and SAP4 in a dose-dependent manner, which might suggest that Cr(VI) caused reproductive toxicity by affecting gene expression. Significant changes in the histological structure of gonad were observed. The results demonstrate that Cr(VI) significantly affected functional and molecular parameters in Geloina coaxans, and indicate that gonad represents the target of exposure to Cr(VI).

Structural Changes Induced by Potassium Dichromate in Renal Cortex of Adult Male Albino Rats and the Possible Protective Role of Selenium

AbstractBackground: Potassium Dichromate (Cr) is a common environmental agent that has been considered potentially carcinogenic, making it an issue of major environmental and search concern.Aim of Study: The aim of this study was to throw light on the possible structural changes in the renal cortex of adult male albino rats after administration of Cr and to elucidate the possibility of protection by selenium (Se) against the deleterious effects of Cr.Material and Methods: Thirty six adult male albino rats weighing 200-230g were divided equally into four groups as follow: Group I received balanced diet and tap water only; Group II received Se orally 0.25mg/kg b.w/daily; Group III rats were received Cr orally 67mg/kg/daily and Group IV rats were received oral Cr and Se at same previous doses. Animals were sacrificed on day 28.Results: The Cr-treated group showed damage of the renal cortex including capsule and renal interstitium. Masson's trichrome staining showed abundant collagen fibers. The expression of caspase-3 in the cytoplasm showed strong positive immune reaction in group III. Biochemical results showed Cr induced significant increase in blood urea nitrogen (BUN), serum creatinine (SC) and uric acid (UA). While morphometric measurement indicated that Cr induced a sta-tistical significant decrease in rat body weight and diameter of glomeruli when compared with other groups. The Cr-treated group also showed a statistical significant increase in kidney weight, surface area of Bowman space, diameter of the con-voluted tubules, area percentage of collagen fibers and ex-pression of caspase-3. Meanwhile, administration of Se showed some protection against the toxic effect of Cr on renal cortex.Conclusion: It is suggested that administration Se mod-erately improves the deleterious histological and biochemical changes induced by Cr on renal cortex.

Toxic effects of Cr(VI) on the bovine hemoglobin and human vascular endothelial cells: Molecular interaction and cell damage

Hexavalent chromium [Cr(VI)] is the main harmful component in the atmosphere released by chemical industry. The study was conducted to assess Cr(VI) inducing cardiovascular diseases (CVDs) in vitro by investigating the effects of Cr(VI) on bovine hemoglobin (BHb) and human umbilical vein endothelial cells (HUVECs). Multi-spectroscopic techniques and molecular docking method were used to determine the interaction of Cr(VI) and BHb. Fluorescence spectra results showed that the quenching constant (Ksv) decreased with temperature raise, indicating that Cr(VI) quenches BHb fluorescence through static quenching mechanism. The number of binding sites was 1.14 (310 K), enthalpy and entropy changes revealed the interaction of Cr(VI) and BHb was driven by hydrogen bonds. The results of synchronous fluorescence and circular dichroism (CD) spectra suggested that Cr(VI) could change BHb conformation and influence the microenvironment of Trp and Tyr residues. Moreover, in order to study Cr(VI) induced HUVECs damage, inflammatory factors were detected at the mRNA level, JNK and p38 MAPK pathways were analyzed. The results shown that Cr(VI) could induce mRNA expression of NLRP3, ICAM-1, VCAM-1, TNF-α and IL-1β, and increased intracellular ROS. Furthermore, Cr(VI) could induce oxidative stress in HUVECs, and then activate JNK and p38 MAPK pathways, ultimately lead to apoptosis of HUVECs by activating mitochondrial apoptosis pathways. These results suggested that Cr(VI) might bring about CVDs by both changing the BHb conformation and inducing HUVECs damage.

Remediation of phytotoxic effect of chromium by different amendments in berseem crop grown in sewage and tubewell water irrigated soils

A screen house experiment was carried out to study the direct effect of chromium(Cr) application in the presence and absence of amendments in berseem crop grown on sewage and tube well water irrigated soils with three replications under factorial completely randomized block design. The results indicated that berseem dry matter yield (DMY) decreased significantly due to direct effect of Cr application but the presence of amendments increased the dry matter yield up to 80 mg/Kg of applied Cr. No harvestable yield was obtained at higher levels of chromium application. The chromium content and chromium uptake also increased significantly with increase in levels of applied chromium. The application of amendments decreased the chromium content and uptake. The toxic effect of Cr on crop could be mitigated more effectively with FYM application than lime and reduce risk of health hazards for human beings and animals.

The Role of Epigenetics in the Toxic Effects Induced by Hexavalent Chromium

The International Agency for Research on Cancer has classified compounds containing hexavalent chromium [Cr(VI)] as GroupⅠhuman carcinogens. Exposure to Cr(VI) via respiratory tract may affect the respiratory function and even lead to lung cancer. The reactive oxygen species (ROS) induced by long-term low-level chromium exposure could cause oxidative stress and DNA damage. There are three possible mechanisms of Cr(VI)-induced carcinogenesis, which are multistage carcinogenesis, genomic instability, and epigenetic modification. Epigenetic changes could be detected at the early stage of DNA damage, including changes of DNA methylation, histone modification, microRNA, circular RNA, long non-coding RNA, and other epigenetic modifications. This review will focus on the role of epigenetic modification in the toxic effects of Cr(VI) and the association between ROS and epigenetic modifications induced by Cr(VI).