Cadmium-induced Oxidative Damage Research Articles

Screening of differentially expressed RNAs and identifying a ceRNA axis during cadmium-induced oxidative damage in pancreatic β cells

Cadmium, a common metal pollutant, has been demonstrated to induce type 2 diabetes by disrupting pancreatic β cells function. In this study, transcriptome microarray was utilized to identify differential gene expression in oxidative damage to pancreatic β cells following cadmium exposure. The results indicated that a series of mRNAs, LncRNAs, and miRNAs were altered. Of the differentially expressed miRNAs, miR-29a-3p exhibited the most pronounced alteration, with an 11.62-fold increase relative to the control group. Following this, the target gene of miR-29a-3p was identified as Col3a1 through three databases (miRDB, miRTarbase and Tarbase), which demonstrated a decrease across the transcriptome microarray. The upstream target gene of miR-29a-3p was identified as NONMMUT036805, with decreased expression observed in the microarray. Finally, the expression trend of NONMMUT036805/miR-29a-3p/Col3a1 was reversed following NAC pretreatment. This was accompanied by a reduction in oxidative damage indicators, MDA/ROS/GSH-Px appeared to be negatively affected to varying degrees. In conclusion, this study has demonstrated that multiple RNAs are altered during cadmium exposure-induced oxidative damage in pancreatic β cells. The NONMMUT036805/miR-29a-3p/Col3a1 axis has been shown to be involved in this process, which provides a foundation for the identification of potential targets for cadmium toxicity intervention.

Methanolic leaf extract of Vernonia amygdalina mitigates cadmium-induced oxidative stress in the liver and kidney of adult male Wistar rats

ABSTRACT Cadmium is a hazardous metal swiftly generated through industrialization and persists in the environment due to its non-biodegradability. Cadmium induces liver and kidney damage primarily by triggering free radical production causing oxidative stress. This study explored the potential of methanolic extract of Vernonia amygdalina in ameliorating cadmium-induced oxidative stress. Twenty adult male Wistar rats were used for this experiment, with each group consisting of five rats. The first group was the unexposed control group given standard rat chow and distilled water ad libitum while the test groups (II-IV) were orally administered with cadmium at standard doses of 12 mg/kg/BW. Vernonia amygdalina at standard doses of 100 mg/kg/BW and 200 mg/kg/BW was administered to rats in groups III and IV respectively. After 28 days, the rats were euthanized using cervical dislocation and the livers and kidneys were analyzed for histological and mRNA analysis of tumor necrosis factor-alpha (TNF-α) and interleukin-10 (IL-10). The results showed significant pathological changes in the histoarchitecture of the livers and kidneys, indicating oxidative stress and the effectiveness of Vernonia amygdalina, which mitigated cadmium-induced oxidative damage by modulating TNF-α and IL-10 expression and ameliorating the histological alteration seen in the studied organs.

Rutin Nanoparticles Alleviate Cadmium-Induced Oxidative and Immune Damage in Broilers' Bursa of Fabricius via Modulating Hsp70/TLR4/NF-κB Signaling Pathway.

Cadmium (Cd) is a serious environmental pollutant affecting various tissues/organs in broilers and compromising their immunological function and productivity. Therefore, the current study aimed to investigate Cd-induced immunotoxicity and potential immunoprotective effect of rutin nanoparticles (RNPs) in the bursal tissue of broilers. A total number of 150 chicks from the Hubbard breed were randomly divided into 5 groups. Group I was fed on standard basal diet (SD) with normal drinking water (DW), Group II received SD containing RNPs (50mg/kg feed) with DW, Group III fed on SD and DW containing Cd (150mg/L), Group IV co-treated with rutin-enforced SD (50mg/kg diet) and DW containing Cd (150mg/L), and finally, Group V co-supplemented with RNP-enhanced SD (50mg/kg diet) DW containing Cd (150mg/L). Productive performance, economic efficiency, oxidative biomarkers, histopathological changes, and the expression level of TLR-4, HSP-70, caspase 3, NF-κB, Bcl-2, and Bax were assessed in the BF tissue. Cd led to severe production and economic losses in exposed birds with a marked surge of oxidative biomarkers, pro-inflammatory cytokines, and histopathological changes in the bursal tissue which could be explained through upregulation of the Hsp70/TLR4/NF-κB molecular pathway in the BF tissue. Meanwhile, RNPs could alleviate most of these changes and prevail optimistic immunomodulatory properties which subsequently could enhance broilers' productivity when incorporated in their diets.

Integrated transcriptome and metabolome analysis provide insights into the mechanism of saponin biosynthesis and its role in alleviating cadmium-induced oxidative damage in Ophiopogon japonicum

Zhe-Maidong, a cultivar of Ophiopogon japonicus is a prominent traditional herbal medicine rich in saponins. This study explored the mechanism of saponin biosynthesis and its role in alleviating Cd-induced oxidative damage in the Zhe-Maidong cultivar using three experimental groups undergoing Cd stress. In the Cd-contaminated soil treatment, total saponins were 1.68 times higher than those in the control. The saponin content in the Cd-2 and Cd-3 treatments was approximately twice as high as that in the Cd-CK treatment. These findings revealed that Cd stress leads to total saponin accumulation. Metabolomic analysis identified the accumulated saponins, primarily several monoterpenoids, diterpenoids, and triterpenoids. The increased saponins exhibited an antioxidant ability to prevent the accumulation of Cd-induced reactive oxygen species (ROS). Subsequent saponin application experiments provided strong evidence that saponin played a crucial role in promoting superoxide dismutase (SOD) activity and reducing ROS accumulation. Transcriptome analysis revealed vital genes for saponin synthesis under Cd stress, including SE, two SSs, and six CYP450s, positively correlated with differentially expressed metabolite (DEM) levels in the saponin metabolic pathway. Additionally, the TF-gene regulatory network demonstrated that bHLH1, bHLH3, mTERF, and AUX/IAA transcript factors are crucial regulators of hub genes involved in saponin synthesis. These findings significantly contribute to our understanding of the regulatory network of saponin synthesis and its role in reducing oxidative damage in O. japonicum when exposed to Cd stress.

Changes of LncRNAs during the Process of Antioxidants Antagonize Cadmium-Induced Oxidative Damage in Islet β Cells.

Long non-coding RNAs (LncRNAs) play important regulatory roles in oxidative damage. Resveratrol, curcumin, and cyanidin are phytogenic antioxidants widely existing in nature and they have been proved to antagonize certain heavy metal-induced oxidative damage in cells. However, can they antagonize oxidative damage induced by cadmium in islet β cells? Are their mechanisms of antagonizing oxidative damage related to LncRNAs? In this study, we first detected the cell viability of each group by CCK8 assay. Next, reactive oxygen species (ROS) were detected by the fluorescent probe. The contents of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD) were detected according to the instructions of corresponding kits. At last, the levels of LncRNAs were detected by fluorescence quantitative real-time polymerase chain reaction (qPCR). The results showed that resveratrol, curcumin and cyanidin were able to reverse the reduction of cell viability induced by cadmium (CdSO4). Further determination revealed that SOD activities of the resveratrol+CdSO4, curcumin+CdSO4, and cyanidin+CdSO4 treatment groups increased significantly, and ROS levels and MDA contents dramatically decreased when compared with single CdSO4-treated group. More importantly, the levels of three CdSO4-elevated LncRNAs (NONMMUT029382, ENSMUST00000162103, ENSMUST00000117235) were all decreased and levels of three CdSO4-inhibited LncRNAs (NONMMUT036805, NONMMUT014565, NONMMUT065427) were increased after the pretreatment of resveratrol, curcumin and cyanidin. In summary, resveratrol, curcumin and cyanidin may effectly reverse the cadmium-induced oxidative damage and suggest that phytogenic antioxidants may prevent cells from cadmium-induced oxidative damage through changing the levels of LncRNAs.

Alleviation of cadmium-induced oxidative damage through application of zinc oxide nanoparticles and strigolactones in Solanum lycopersicum L.

In this research, zinc oxide nanoparticles (ZnO NPs) are bio-synthesized using Mangifera indica leaf extract and used for reduction of cadmium (Cd) stress in tomato plants.

Effect of Spirulina maxima microcapsules to mitigate testicular toxicity induced by cadmium in rats: Optimization of in vitro release behavior in the milk beverage

The research investigates the effects of freeze-dried Spirulina maxima microcapsules in reducing testicular toxicity in rats and optimizing the in vitro release behavior of milk beverages using response surface methodology (RSM). Particle size, polydispersity index and zeta-potential were impacting microcapsules’ stability and bioactivity. Thirty-six male Sprague-Dawley rats were utilized; eighteen of them received cadmium orally at a dose of 0.5 mg/mL/rat/d. The nutritional and biochemical parameters were evaluated. Non-encapsulated and Spirulina maxima microcapsules exhibited no significant adverse consequences in vitro experiment. Spirulina maxima microcapsules defended rats against both the inflammatory and apoptotic consequences triggered by cadmium. Incorporating Spirulina maxima microcapsules into the milk beverage at 3 % optimized in vitro release behavior of antioxidants and phenolics due to the increasing importance of these compounds' biological activity. Spirulina maxima microcapsules guide as a viable approach for providing nutritional enrichment in the food industry; moreover, protecting against cadmium-induced oxidative testicular damage in rats.

Physiological and biochemical mechanisms of brassinosteroid in improving anti-cadmium stress ability of Panax notoginseng

In this study, the effect of brassinosteroid(BR) on the physiological and biochemical conditions of 2-year-old Panax notoginseng under the cadmium stress was investigated by the pot experiments. The results showed that cadmium treatment at 10 mg·kg~(-1) inhibited the root viability of P. notoginseng, significantly increased the content of H_2O_2 and MDA in the leaves and roots of P. noto-ginseng, caused oxidative damage of P. notoginseng, and reduced the activities of SOD and CAT. Cadmium stress reduced the chlorophyll content of P. notoginseng, increased leaf F_o, reduced F_m, F_v/F_m, and PIABS, and damaged the photosynthesis system of P. notoginseng. Cadmium treatment increased the soluble sugar content of P. notoginseng leaves and roots, inhibited the synthesis of soluble proteins, reduced the fresh weight and dry weight, and inhibited the growth of P. notoginseng. External spray application of 0.1 mg·L~(-1) BR reduced the H_2O_2 and MDA content in P. notoginseng leaves and roots under the cadmium stress, alleviated cadmium-induced oxidative damage to P. notoginseng, improved the antioxidant enzyme activity and root activity of P. notoginseng, increased the content of chlorophyll, reduced the F_o of P. notoginseng leaves, increased F_m, F_v/F_m, and PIABS, alleviated the cadmium-induced damage to the photosynthesis system, and improved the synthesis ability of soluble proteins. In summary, BR can enhance the anti-cadmium stress ability of P. notoginseng by regulating the antioxidant enzyme system and photosynthesis system of P. notoginseng under the cadmium stress. In the context of 0.1 mg·L~(-1) BR, P. notoginseng can better absorb and utilize light energy and synthesize more nutrients, which is more suitable for the growth and development of P. notoginseng.

Determinants of oxidative stress among indigenous populations in Northern Laos: Trace element exposures and dietary patterns

ObjectivesTo investigate determinants of oxidative stress in an indigenous population, we examined associations of trace element exposures and dietary patterns with three oxidative stress-related biomarkers among indigenous populations in Northern Laos. MethodsThis cross-sectional study included 341 adults from three villages with different levels of modernization. We used three oxidative stress-related biomarkers: urinary 8-hydroxy-2′-deoxyguanosine (8-OHdG) and 8-isoprostane concentrations, which were measured using liquid chromatography-tandem mass spectrometry, and blood telomere lengths, which were measured using a quantitative polymerase chain reaction method. We used multilevel analysis to examine associations of urinary arsenic, cadmium, and selenium concentrations, their interaction terms, and wild-plant-food scores (principal component scores calculated from food consumption frequencies) with oxidative stress-related biomarkers. ResultsUrinary arsenic and cadmium concentrations were positively associated with urinary 8-isoprostane concentrations. Urinary selenium concentrations were positively associated with urinary 8-OHdG concentrations. Interaction terms ([arsenic or cadmium] × selenium) showed negative associations with urinary 8-OHdG and 8-isoprostane concentrations, respectively. Urinary cadmium concentrations were negatively associated with telomere lengths. Wild-plant-food scores did not exhibit associations with oxidative stress-related biomarkers. ConclusionOur findings imply that exposure to arsenic and cadmium is associated with greater oxidative lipid damage, whereas selenium may attenuate arsenic-induced oxidative DNA damage and cadmium-induced oxidative lipid damage. Cadmium exposure may accelerate telomere attrition. Trace element exposure may be a determinant of oxidative stress among indigenous populations in Northern Laos.

Alleviating effect of quercetin on cadmium-induced oxidative damage and apoptosis by activating the Nrf2-keap1 pathway in BRL-3A cells.

Cadmium (Cd) is a toxic heavy metal extensively used in industrial and agricultural production. Among the main mechanisms of Cd-induced liver damage is oxidative stress. Quercetin (QE) is a natural antioxidant. Herein, the protective effect of QE on Cd-induced hepatocyte injury was investigated. BRL-3A cells were treated with 12.5 μmol/L CdCl2 and/or 5 μmol/L QE for 24 h. The cells and medium supernatant were collected, and the ALT, AST, and LDH contents of the medium supernatant were detected. The activities or contents of SOD, CAT, GSH, and MDA in cells were determined. Intracellular ROS levels were examined by flow cytometry. Apoptosis rate and mitochondrial-membrane potential (ΔΨm) were detected by Hoechst 33,258 and JC-1 methods, respectively. The mRNA and protein expression levels of Nrf2, NQO1, Keap1, CytC, caspase-9, caspase-3, Bax, and Bcl-2 were determined by real-time PCR (RT-PCR) and Western blot methods. Results showed that Cd exposure injured BRL-3A cells, the activity of antioxidant enzymes decreased and the cell ROS level increased, whereas the ΔΨm decreased, and the expression of apoptotic genes increased. Cd inhibited the Nrf2-Keap1 pathway, decreased Nrf2 and NQO1, or increased Keap1 mRNA and protein expression. Through the combined action of Cd and QE, QE activated the Nrf2-Keap1 pathway. Consequently, antioxidant-enzyme activity decreased, cellular ROS level decreased, ΔΨm increased, Cd-induced BRL-3A cell damage was alleviated, and cell apoptosis was inhibited. After the combined action of QE and Cd, Nrf2 and NQO1 mRNA and protein expression increased, Keap1 mRNA and protein expression decreased. Therefore, QE exerted an antioxidant effect by activating the Nrf2-Keap1 pathway in BRL-3A cells.

Amelioration of Cadmium-Induced Oxidative Damage in Wistar Rats by Vitamin C, Zinc and N-Acetylcysteine.

The present study was performed to determine the protective effects of vitamin C, zinc, and N-acetylcysteine, individually or in combination with Cd, to monitor their amelioration capability against Cd-induced oxidative damage in Wistar rats. We investigated and demonstrated that cadmium is a toxic element that damages rat liver and kidney tissues. Vitamin C, zinc, and NAC have been proven to have protective roles against Cd toxic effects. Nine groups of rats were studied as the experimental group. The present experiment was conducted for 45 days. Liver and kidneys were excised for biochemical evaluation by assaying antioxidant enzymes and lipid oxidation products to assess the impact of Cd toxicity and its amelioration by co-administration of vitamin C, zinc, and NAC along with Cd. Basal metabolic rates and tissue respiration rates of liver and kidney were significantly decreased (p < 0.05) during Cd toxicity. Serum biochemical parameters were also found to be significantly altered to cope with Cd toxicity. All the antioxidant enzymes and products were significant inhibited (p < 0.05) or elevated in rat liver and kidney tissues during Cd-induced toxicity. Our results suggest that co-administration of vitamin C, zinc, and NAC to rats ameliorates oxidative damage induced by Cd toxicity. From the results obtained in the present study, all the agents tested had protective effects against Cd-induced oxidative damage.

Honokiol Attenuates Hepatic Endosome-Lysosomal Vacuolation by Attenuating Cadmium-Induced Oxidative Stress and Mitochondrial Damage in Quail Livers

Honokiol Attenuates Hepatic Endosome-Lysosomal Vacuolation by Attenuating Cadmium-Induced Oxidative Stress and Mitochondrial Damage in Quail Livers

Puerarin alleviates cadmium-induced oxidative damage to bone by reducing autophagy in rats.

Autophagy is a regulatory mechanism involved in cadmium (Cd)-induced bone toxicity and is suppressed by various stimuli, including oxidative stress. Puerarin is an isoflavonoid compound isolated from Pueraria, a plant used in traditional Chinese medicine. The underlying mechanisms of action of puerarin remain unclear. The objective of this study was to explore the mitigating effects of puerarin on cadmium-induced oxidative damage in the bones of rats. Cadmium exposure increased oxidative damage in rat bones; this was markedly decreased by puerarin treatment, as demonstrated by changes in the activity of antioxidative enzymes. Cadmium-induced blockage of the expression of key bone regulatory proteins, autophagy-related markers, and signaling molecules was also alleviated by puerarin treatment. Additionally, cadmium reduced expression of the autophagic protein Rab7 and of late endosomal/lysosomal adaptor and MAPK and mTOR activator 1 (LAMTOR1); the decrease in these proteins was not restored by puerarin treatment. We speculate that puerarin relieves the inhibition of fusion of autophagosomes with lysosomes that is induced by cadmium; however, this specific effect of puerarin and downstream effects on bone regulatory mechanisms require further investigation. In conclusion, puerarin alleviates cadmium-induced oxidative damage in the bones of rats by attenuating autophagy, which is likely associated with the antioxidant activity of puerarin.

Arctigenin alleviates cadmium-induced nephrotoxicity: Targeting endoplasmic reticulum stress, Nrf2 signaling, and the associated inflammatory response

AimNephrotoxicity is a critical consequence of cadmium toxicity. Cadmium induces nephrotoxicity through disruption of cellular redox balance and induction of endoplasmic reticulum stress (ERS) and inflammatory responses. The present study investigated the renoprotective effects of the naturally occurring arctigenin against the cadmium-induced nephrotoxicity. Main methodsMale Wistar rats were randomized into normal control, arctigenin control, cadmium, and cadmium/arctigenin groups. Cadmium and arctigenin were administered daily over a seven-day period. On the eighth day, blood and kidney tissue specimens were collected and subjected to spectrophotometric, ELISA, and immunoblotting analysis. Key findingsArctigenin significantly improved renal functions and reduced renal tubular injury in the cadmium-intoxicated rats as reflected by increased GFR and reduced levels of serum creatinine, BUN, urinary albumin-to-creatinine ratio, and protein expression of KIM-1. Arctigenin alleviated the cadmium-induced oxidative DNA damage and lipid peroxidation while boosted reduced glutathione level and antioxidant enzymes activity. Mechanistically, arctigenin enhanced nuclear translocation of the antioxidant transcription factor Nrf2 and up-regulated its downstream redox-regulating enzymes HO-1 and NQO1. Importantly, arctigenin ameliorated the cadmium-evoked ERS as demonstrated by reduced protein expression of the key molecules Bip, PERK, IRE1α, CHOP, phspho-eIF2α, and caspase-12 and diminished activity of caspase-12. Additionally, arctigenin down-regulated the cadmium-induced NF-κB nuclear translocation and decreased its downstream pro-inflammatory cytokines TNF-α and IL-1β. SignificanceThe current work underlines the alleviating activity of arctigenin against cadmium-evoked nephrotoxicity potentially through mitigating ERS and targeting Nrf2 and NF-κB signaling. The current findings support possible therapeutic application of arctigenin in controlling cadmium-induced nephrotoxicity although clinical investigations are necessary.

L-arginine Ameliorated Mitochondrial Oxidative Damage Induced by Sub-chronic Exposure to Cadmium in Mice Kidney

Background:Cadmium is a heavy metal that can cause various injuries in the body, including nephrotoxicity. L-Arginine is a metal chelator that can prevent oxidative damage caused by oxygen free radicals.&#x0D; Objectives:This study aimed to investigate the effect of L-arginine in inhibiting mitochondrial toxicity induced by subchronic cadmium exposure in the kidney of male mice.&#x0D; Methods: A total of 42 male mice were randomly divided into six groups (n=6): control (normal saline), cadmium (2 mg/kg), cadmium (2 mg/kg) plus three doses of L-arginine (50, 100, and 200 mg/kg) and finally cadmium (2 mg/kg) plus vitamin C (500 mg/kg). After 42 days, the animals were anesthetized with ketamine/xylazine. Their kidney tissues were removed, and mitochondrial fractions were isolated. Oxidative stress factors and mitochondrial damage parameters (MTT, swelling, and mitochondrial membrane potential) were measured in renal isolated mitochondria. Also, evaluation of Blood Urea Nitrogen (BUN) and Creatinine (Cr) tests were done.&#x0D; Results: Significant rise in BUN and Cr were observed in cadmium-treated mice (P&lt;0.05). Cadmium enhanced oxidative stress in the kidney via increasing lipid peroxidation and oxidation of protein and glutathione. It caused significant mitochondrial dysfunction, mitochondrial membrane potential collapse, and swelling in isolated mitochondria (P&lt;0.05). L-Arginine significantly ameliorated cadmium-induced oxidative stress and mitochondrial damage (P&lt;0.05). Furthermore, a significant reduction in serum BUN and Cr were observed in L-arginine received group (P&lt;0.05).&#x0D; Conclusion: The results showed that L-arginine has significant protective effects against cadmium-induced renal toxicity in male mice.

Bioactive phytochemicals from Salvia officinalis attenuate cadmium-induced oxidative damage and genotoxicity in rats.

This study was conducted to identify the bioactive phytochemicals in Salvia officinalis essential oil, to determine the polyphenols in the aqueous extract (SOE), and to evaluate their protective role against cadmium (Cd)-induced oxidative damage and genotoxicity in rats. Six groups of female rats were treated orally for 2 weeks including the control group, CdCl2-treated group, SOE-treated groups at low or high dose (100 and 200 mg/kg b.w), and CdCl2 plus SOE-treated groups at the two doses. The GC-MS analysis identified 39 compounds; the main compounds were 9-octadecenamide, eucalyptol, palmitic acid, and oleic acid. However, the HPLC analysis showed 12 polyphenolic compounds and the majority were coumaric acid, chlorogenic acid, coffeic acid, catechin, vanillin, gallic acid, ellagic acid, and rutin. In the biological study, rats received CdCl2 displayed severe disturbances in liver and kidney indices alanine aminotransferase (ALT), aspartate aminotransferase (AST), albumin (Alb), total protein (TP), total bilirubin (T. Bil), direct bilirubin (D. Bil), creatinine, uric acid, and urea, lipid profile, tumor necrosis factor-alpha (TNF-α), alpha-fetoprotein (AFP) and CEA), glutathione (GSH), glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (CAT), malondialdehyde (MDA), nitric oxide (NO), gene expressions, DNA fragmentation, and histological alterations in the liver and kidney tissue. SOE showed a potent antioxidant and mitigated these alterations in serum and tissue. Moreover, the high dose succeeded to normalize most of the tested parameters and histological features. It could be concluded that S. officinalis is a promising source for bioactive compounds with therapeutic benefits against environmental toxicants.

Ameliorative Effects of Exogenous Proline on Photosynthetic Attributes, Nutrients Uptake, and Oxidative Stresses under Cadmium in Pigeon Pea (Cajanus cajan L.).

Proline plays a significant role in the plant response to stress conditions. However, its role in alleviating metal-induced stresses remains elusive. We conducted an experiment to evaluate the ameliorative role of exogenous proline on cadmium-induced inhibitory effects in pigeon pea subjected to different Cd treatments (4 and 8 mg/mL). Cadmium treatments reduced photosynthetic attributes, decreased chlorophyll contents, disturbed nutrient uptake, and affected growth traits. The elevated activity of antioxidant enzymes (superoxide dismutase, catalase, and glutathione peroxidase), in association with relatively high contents of hydrogen peroxide, thiobarbituric acid reactive substances, electrolyte leakage, and endogenous proline, was measured. Exogenous proline application (3 and 6 mM) alleviated cadmium-induced oxidative damage. Exogenous proline increased antioxidant enzyme activities and improved photosynthetic attributes, nutrient uptake (Mg2+, Ca2+, K+), and growth parameters in cadmium-stressed pigeon pea plants. Our results reveal that proline supplementation can comprehensively alleviate the harmful effects of cadmium on pigeon pea plants.

Changes and relationship of N6-methyladenosine modification and long non-coding RNAs in oxidative damage induced by cadmium in pancreatic β-cells

N6-methyladenosine (m6A) modification and m6A-modified Long non-coding RNAs (LncRNAs) play crucial roles in various pathological processes, yet their changes and relationship in cadmium-induced oxidative damage are largely unknown. Here, five m6A-modified LncRNAs (LncRNA-TUG1, LncRNA-PVT1, LncRNA-MALAT1, LncRNA-XIST, LncRNA-NEAT1), which have been evidenced to involve in oxidative damage, were selected and their binding proteins were submitted to bioinformatics analysis. Our analysis results showed that these five m6A-modified LncRNAs bound to different regulatory proteins of m6A modification, implicating that m6A modification on LncRNAs may synergistically control by multiple regulatory proteins. Furthermore, the detection data revealed that levels of m6A modification, methyltransferase-like 3 (METTL3) and fat mass and obesity-associated protein (FTO) were all significantly decreased in CdSO4-induced oxidative damage, which was demonstrated by increasing ROS accumulation and MDA contents as well as decreasing SOD activities. More importantly, LncRNA-MALAT1 and LncRNA-PVT1 indicated downward trend and showed positive relationship with m6A modification. Collectively, our results showed that m6A modification and m6A-modified LncRNAs may involve in oxidative damage induced by cadmium.

Dietary supplementation with manganese and selenium offer protection against cadmium-induced oxidative damage to rat liver and kidney

The present study determined the effect of pre-supplementation with manganese (Mn) and selenium (Se) on biomarkers of oxidative stress in the liver and kidneys of rats exposed to a mild dose of cadmium. Sixteen Male Wistar strain rats (180-200 g b. wt) were divided into four groups (control, Cd alone, Mn + Se + Cd and Mn + Se). The rats used as the control received a normal rat diet and tap water throughout the study while the Cd alone rats received a normal rat diet and then exposed to a single daily oral dose of cadmium (3 mg CdCl2/kg) in drinking water for three days. Mn + Se + Cd rats were pretreated with Mn (3 mg MnCl2/kg/day) and Se (3mg SeO2/kg/day) for seven days and thereafter received a single daily oral dose of cadmium (3 mg CdCl2/kg) in drinking water for three days while Mn + Se rats were exposed to only Mn (3 mg MnCl2/kg/day) and Se (3mg SeO2/kg/day) for seven days. At the end of the experiment tissue cadmium concentration, membrane lipid peroxidation, glutathione content, and activities of antioxidant enzymes catalase, superoxide dismutase, and glutathione peroxidase were determined in the liver and kidney samples. The results showed that pretreatment with Mn and Se effectively countered Cd-induced cadmium accumulation, membrane lipid peroxidation, depletion of the non-enzymic antioxidant, glutathione, and induction of the antioxidant enzymes catalase, superoxide dismutase and glutathione peroxidase in the liver and kidney. It can be concluded that pre-supplementation with Mn and Se significantly reversed Cd-induced deleterious alterations in the liver and kidney tissue of the rats.

Dietary supplementation with manganese and selenium offer protection against cadmium-induced oxidative damage to rat liver and kidney

Dietary supplementation with manganese and selenium offer protection against cadmium-induced oxidative damage to rat liver and kidney