Cadmium-induced Oxidative Stress Research Articles

Protective Effects of Ascorbic Acid Against Cadmium-Induced Toxicity in the Placenta and Fetus of Rats.

This study aimed to determine the protective role of l-ascorbic acid in a pregnant rat model of cadmium-induced toxicity. Cadmium is a toxic heavy metal that can seriously harm placenta and fetus tissue in pregnant women. Forty-two healthy female Wistar albino rats (250-300 g weight and 14-16 weeks) were randomly distributed into six equal groups (n = 7): control, cadmium 1 mg (CD1), cadmium 5 mg (CD5), ascorbic acid (AA), CD1+AA, CD5+AA. Cadmium was administered to pregnant rats by oral gavage every other day, and/or AA (200 mg) was administered every day. At the end of pregnancy (Day 21), blood, placenta, and fetuses were collected from rats. The results indicated that cadmium-induced oxidative stress by increasing the level of MDA and by decreasing the levels of GSH, SOD, and CAT activity in the serum of maternal. However, AA administration significantly decreased MDA levels and increased GSH levels, SOD, and CAT activity (p < 0.05). Cadmium (5 mg/kg) exposure significantly increased creatinine levels compared to AA and CD1+AA groups (p < 0.05). In addition, AA (200 mg/kg) significantly attenuated cadmium-induced histopathological alteration in the placental and fetal tissues. In conclusion, AA may prevent cadmium toxicity in maternal and fetal tissues, as it regulates oxidative imbalance in pregnant rat tissues and alleviates histopathological changes.

Lactic acid bacteria supplementation: A bioprotective approach to mitigating cadmium-induced toxicity and modulating gene expression in murine models

This study aimed to assess the effects of different strains of lactic acid bacteria, namely LeviLactobacillus brevis (AC10), Lacticaseibacillus rhamnosus (AC11), and Pediococcus acidilactici (AC15), on mice exposed to cadmium-induced oxidative stress. The study assessed weight gain, liver enzymes, antioxidant enzymes, immunoglobulin factors, lipid peroxidation, and gene expression in liver and brain of mice. The findings revealed that the AC10 and AC11 strains had a higher ability to absorb Cd as compared to AC15. The in vivo analysis demonstrated that the dietary dual supplementation of AC10 and AC11 resulted in significant (p < 0.05) improvements, including increased body weight and food intake, reduced cadmium tissue deposition, decreased lipid peroxidation, enhanced cellular antioxidant redox potential, suppressed inflammation genes in the liver and brain tissues, and improved morpho-characteristics of the jejunum in mice challenged by cadmium-induced toxicity. The multiple mechanisms of action, including heavy metal sequestration, antioxidant enhancement, and maintenance of intestinal integrity, highlight the potential of these probiotics’ intervention as a viable approach to counteract the deleterious effects of cadmium exposure.

Transcription factors involved in plant responses to cadmium-induced oxidative stress

Cadmium (Cd) is a heavy metal highly toxic to living organisms. Cd pollution of soils has become a serious problem worldwide, posing a severe threat to crop production and human health. When plants are poisoned by Cd, their growth and development are inhibited, chloroplasts are severely damaged, and respiration and photosynthesis are negatively affected. Therefore, elucidating the molecular mechanisms that underlie Cd tolerance in plants is important. Transcription factors can bind to specific plant cis-acting genes. Transcription factors are frequently reported to be involved in various signaling pathways involved in plant growth and development. Their role in the resistance to environmental stress factors, particularly Cd, should not be underestimated. The roles of several transcription factor families in the regulation of plant resistance to Cd stress have been widely demonstrated. In this review, we summarize the mechanisms of five major transcription factor families–WRKY, ERF, MYB, bHLH, and bZIP–in plant resistance to Cd stress to provide useful information for using molecular techniques to solve Cd pollution problems in the future.

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.

Crosstalk between melatonin and nitric oxide restrains Cadmium-induced oxidative stress and enhances vinblastine biosynthesis in Catharanthus roseus (L) G Don.

Nitric oxide functions downstream of the melatonin in adjusting Cd-induced osmotic and oxidative stresses, upregulating the transcription of D4H and DAT genes, and increasing total alkaloid and vincristine contents. A few studies have investigated the relationship between melatonin (MT) and nitric oxide (NO) in regulating defensive responses. However, it is still unclear how MT and NO interact to regulate the biosynthesis of alkaloids and vincristine in leaves of Catharanthus roseus (L.) G. Don under Cd stress. Therefore, this context was explored in the present study. Results showed that Cd toxicity (200µM) induced oxidative stress, decreased biomass, Chl a, and Chl b content, and increased the content of total alkaloid and vinblastine in the leaves. Application of both MT (100µM) and sodium nitroprusside (200µM SNP, as NO donor) enhanced endogenous NO content and accordingly increased metal tolerance index, the content of total alkaloid and vinblastine. It also upregulated the transcription of two respective genes (D4H and DAT) under non-stress and Cd stress conditions. Moreover, the MT and SNP treatments reduced the content of H2O2 and malondialdehyde, increased the activities of superoxide dismutase and ascorbate peroxidase, enhanced proline accumulation, and improved relative water content in leaves of Cd-exposed plants. The scavenging NO by 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxy l-3-oxide (cPTIO) averted the effects of MT on the content of total alkaloid and vinblastine and antioxidative responses. Still, the effects conferred by NO on attributes mentioned above were not significantly impaired by p-chlorophenylalanine (p-CPA as an inhibitor of MT biosynthesis). These findings and multivariate analyses indicate that MT motivated terpenoid indole alkaloid biosynthesis and mitigated Cd-induced oxidative stress in the leaves of periwinkle in a NO-dependent manner.

Cadmium biosorption: Lake waters in Bengaluru-mitigation of cadmium-induced oxidative stress by Selaginella bryopteris

ABSTRACT Heavy metals cause alarming levels of environmental and health problems and among them Cadmium has become a threat to organisms and natural resources like soil and water alike. It accumulates in living systems thereby causing oxidative stress. Efforts are made for bioremediation of heavy metals by employing biosorption, which is a well-known economic method for removal and in the current study Selaginella bryopteris was used as biosorbent. The biosorption capacity was optimized by its physicochemical parameters such as pH, dosage, contact time, and temperature. Cadmium-induced Reactive Oxygen Species levels and the antioxidant potential of S. bryopteris in ameliorating them were studied in Drosophila melanogaster. Water-quality analysis was performed using Chemical Oxygen Demand(COD) and Biological Oxygen Demand (BOD) and effect of S.bryopteris on these parameters were also analyzed. Further the concentration of Cadmium via colorimetric assay and Atomic Absorption Spectroscopy(AAS) was employed to quantify the Cadmium in lake water samples before and after treatment with biosorbent. Fourier Transform Infrared Spectroscopy (FTIR) and Scanning Electron Microscope (SEM) were performed to characterize the surface properties for adsorptive removal of metal ions, and antioxidant studies were conducted to assess the role of S. bryopteris in suppressing oxidative stress.

Antioxidant Effects of Whey Protein as a Dietary Supplement to Alleviate Cadmium-Induced Oxidative Stress in Male Wistar Rats

The liquid whey is a byproduct produced during cheese making. Cadmium is a highly hazardous heavy metal with cumulative toxic effects. The present research work was done to clarify the possible role of whey proteins in alleviating cadmium-induced oxidative stress. The used rats were allotted equally and randomly into three experimental groups; untreated control, cadmium-exposed, and cadmium-exposed and whey protein-administered groups. The biochemical and haematological assays of rats exposed to cadmium (group 2) manifested significant alterations compared to those of untreated control animals. Concerning the biochemical serum profile, group 3 animals showed relatively increased levels of total proteins, significant increments of total thiols, glutathione, total antioxidant capacity (TAC), and catalase, and significant decrements in the levels of blood cadmium, alanine transferase (ALT), aspartate transferase (AST), alkaline phosphatase (ALP), creatinine, urea, bilirubin, hydrogen peroxide (H2O2), and malondialdehyde (MDA) compared to the animals exposed to cadmium (group 2). Homogenates of liver and kidney tissues obtained from group 3 animals demonstrated similar results to that revealed by the serum assay. It was concluded that whey proteins as a dietary supplement can offer potential antioxidant properties that enable these supplementary proteins to alleviate cadmium-induced oxidative stress.

The antagonism mechanism of astilbin against cadmium-induced injury in chicken lungs via Treg/Th1 balance signaling pathway

The purpose of this study was to investigate the effect of Treg/Th1 imbalance in cadmium-induced lung injury and the potential protective effect of astilbin against cadmium-induced lung injury in chicken. Cadmium exposure significantly decreased T-AOC and GSH-Px levels and SOD activity in the chicken lung tissues. In contrast, it significantly increased the MDA and NO levels. These results indicate that cadmium triggers oxidative stress in lungs. Histopathological analysis revealed that cadmium exposure further induced infiltration of lymphocytes in the chicken lungs, indicating that cadmium causes pulmonary damage. Further analysis revealed that cadmium decreased the expression of IL-4 and IL-10 but increased those of IL-17, Foxp3, TNF-α, and TGF-β, indicating that the exposure of cadmium induced the imbalance of Treg/Th1. Moreover, cadmium adversely affected chicken lung function by activating the NF-kB pathway and inducing expression of genes downstream to these pathways (COX-2, iNOS), associated with inflammatory injury in the lung tissue. Astilbin reduced cadmium-induced oxidative stress and inflammation in the lungs by increasing antioxidant enzyme activities and restoring Treg/Th1 balance. In conclusion, our results suggest that astilbin treatment alleviated the effects of cadmium-mediated lung injury in chickens by restoring the Treg/Th1 balance.

Synergistic interplay between melatonin and hydrogen sulfide enhances cadmium-induced oxidative stress resistance in stock (Matthiola incana L.)

ABSTRACT Ornamental crops particularly cut flowers are considered sensitive to heavy metals (HMs) induced oxidative stress condition. Melatonin (MLT) is a versatile phytohormone with the ability to mitigate abiotic stresses induced oxidative stress in plants. Similarly, signaling molecules such as hydrogen sulfide (H2S) have emerged as potential options for resolving HMs related problems in plants. The mechanisms underlying the combined application of MLT and H2S are not yet explored. Therefore, we evaluated the ability of individual and combined applications of MLT (100 μM) and H2S in the form of sodium hydrosulfide (NaHS), a donor of H2S, (1.5 mM) to alleviate cadmium (Cd) stress (50 mg L−1) in stock (Matthiola incana L.) plants by measuring various morpho-physiological and biochemical characteristics. The results depicted that Cd-stress inhibited growth, photosynthesis and induced Cd-associated oxidative stress as depicted by excessive ROS accumulation. Combined application of MLT and H2S efficiently recovered all these attributes. Furthermore, Cd stress-induced oxidative stress markers including electrolyte leakage, malondialdehyde, and hydrogen peroxide are partially reversed in Cd-stressed plants by MLT and H2S application. This might be attributed to MLT or H2S induced antioxidant plant defense activities, which effectively reduce the severity of oxidative stress indicators. Overall, MLT and H2S supplementation, favorably regulated Cd tolerance in stock; yet, the combined use had a greater effect on Cd tolerance than the independent application.

Anthocyanins from Lycium ruthenicum Murray Mitigate Cadmium-Induced Oxidative Stress and Testicular Toxicity by Activating the Keap1/Nrf2 Signaling Pathway.

Cadmium (Cd) is a hazardous heavy metal environmental pollutant that has carcinogenic, teratogenic, and mutagenic properties. Excessive exposure to Cd can induce oxidative stress, which greatly harms the male reproductive system. Anthocyanins have remarkable antioxidative, anti-inflammatory, and anti-stress properties. In this study, we investigated the effects of anthocyanins and the underlying mechanisms through which anthocyanins mitigate Cd-induced reproductive damage. We isolated and purified Lycium ruthenicum Murray anthocyanin extract (LAE) and performed UHPLC-MS/MS to identify 30 different anthocyanins. We established an ICR mouse Cd injury model by administering 5 mg/kg/day CdCl2 for 28 consecutive days. LAE at 500 mg/kg/day effectively ameliorated testicular damage and preserved spermatogenesis. The mice in the LAE-treated group had elevated testosterone and inhibin B levels. Additionally, the treatment restored the activity of antioxidant enzymes, including T-SOD, CAT, and GR, and substantially increased the levels of the non-enzymatic antioxidant GSH. Research findings indicate that LAE can activate the SIRT1/Nrf2/Keap1 antioxidant pathway. This activation is achieved through the upregulation of both the SIRT1 gene and protein levels, leading to the deacetylation of Nrf2. Moreover, LAE reduces the expression of Keap1, alleviating its inhibitory effect on Nrf2. This, in turn, facilitates the uncoupling process, promoting the translocation of Nrf2 to the nucleus, where it governs downstream expression, including that of HO-1 and GPX1. LAE effectively mitigated toxicity to the reproductive system associated with exposure to the heavy metal Cd by alleviating oxidative stress in the testes.

Transcriptome Analysis and Identification of Cadmium-Induced Oxidative Stress Response Genes in Different Meretrix meretrix Developmental Stages.

Cadmium (Cd) is one of the major pollutants in the aquatic environment, and it can easily accumulate in aquatic animals and result in toxic effects by changing the metabolism of the body, causing a serious impact on the immune system, reproductive system, and the development of offspring. The clam Meretrix meretrix is one of the commercially important species that is cultivated in large-scale aquaculture in China. To elucidate the underlying molecular mechanisms of Cd2+ in the developmental processes, fertilized eggs and larvae of M. meretrix at different developmental stages were exposed to Cd2+ (27.2 mg L-1 in natural seawater) or just natural seawater without Cd2+ (control), and high-throughput transcriptome sequencing and immunohistochemistry techniques were used to analyze the toxic effects of Cd on larvae at different early developmental stages. The results revealed 31,914 genes were differentially expressed in the different stages of M. meretrix development upon treatment with Cd2+. Ten of these genes were differentially expressed in all stages of development examined, but they comprised only six unigenes (CCO, Ndh, HPX, A2M, STF, and pro-C3), all of which were related to the oxidative stress response. Under Cd exposure, the expression levels of CCO and Ndh were significantly upregulated in D-shaped and pediveliger larvae, while pro-C3 expression was significantly upregulated in the fertilized egg, D-shaped larva, and pediveliger. Moreover, HPX, A2M, and STF expression levels in the fertilized egg and pediveliger larvae were also significantly upregulated. In contrast, CCO, Ndh, HPX, A2M, STF, and pro-C3 expression levels in the postlarva were all downregulated under Cd exposure. Besides the genes with changes in expression identified by the transcriptome, the expression of two other oxidative stress-related genes (MT and Nfr2) was also found to change significantly in the different developmental stages of M. meretrix upon Cd exposure, confirming their roles in combating oxidative stress. Overall, the findings of this study indicated that Cd would interfere with cellular respiration, ion transport, and immune response through inducing oxidative stress, and changes in the expression of oxidative stress-related genes might be an important step for M. meretrix to deal with the adverse effects of Cd at different stages of its development.

Protective effects of Quercus salicina blume leaves aqueous extracts against cadmium-induced oxidative stress and cell cytotoxicity in HK-2 cells

Background: Quercus salicina Blume is an evergreen plant growing southern parts of Korea and Japan, and has been used for the treatment of dysentery, dermatitis, and hemorrhage from possible effects such as anti-inflammatory, anti-endemic and litholytic activities. We investigated the underlying mechanisms of Quercus salicina Blume leaf extracts (QS) protection against cadmium treatment utilizing human kidney origin HK-2 cells.Methods: To ascertain the functional constituents of the hot water-extracted QS, we conducted analyses to determine the total phenolic and flavonoid contents. Subsequently, the antioxidant activity was assessed using DPPH (2,2-diphenyl-1-picrylhydrazyl) and FRAP (ferric ion reducing antioxidant power) methods. After treating HK-2 cells with QS and Cd, we confirmed the production of reactive oxygen species (ROS) and the expression of related proteins through western blotting. This investigation aimed to assess the antioxidant and anti-apoptotic effects of QS against cadmium-induced oxidative stress. Results: QS exhibited strong antioxidative potential, since the samples exhibited significantly high DPPH and FRAP values. Upon exposure of HK-2 cells to cadmium, inducing oxidative stress, the application of QS effectively reinstated cellular antioxidative functions, leading to an augmentation in cell viability. Notably, the presence of QS attenuated the heightened expression of oxidative marker enzymes induced by cadmium treatment, including SOD (superoxide dismutase) 1, catalase, Nrf-2, and Heme-oxygenase. The apparent disappearance of the apoptotic bodies indicates a potential apoptosis controlling effect of QS. Furthermore, the considerable increase in sub-G1 phase with the addition of cadmium was diminished under QS treatment indicating the ability of QS to reduce the degree of apoptosis related cell cycle phase. The apoptotic quenching effects of QS were accompanied by the downregulation of pro-apoptotic protein Bax and up-regulation of pro-apoptotic Bcl-2. The examination of cleaved caspase-9 and caspase-3 has provided evidence that the pronounced anti-apoptotic activities observed in cadmium-challenged HK-2 cells significantly diminished in the presence of QS. Conclusions: QS is a highly effective antioxidant and reduces cell cytotoxicity caused by cadmium through antioxidant functions and anti-apoptotic capabilities.Keywords: Quercus salicina Blume leave, cadmium, antioxidant, anti-apoptosis

Protective effect of the extract from Aronia melanocarpa L. berries against cadmium-induced oxidative stress in the kidney: A study in an in vivo experimental model

The destructive impact of cadmium (Cd) on the oxidative/antioxidative status of the kidney, as well as the possible beneficial effect of co-administration of a 0.1% aqueous extract from Aronia melanocarpa L. berries (AM), were studied in a rat model of low-level and moderate general population exposure to this heavy metal (1 and 5 mg Cd/kg feed, respectively, for up to 24 months). Total antioxidative status (TAS) of the kidney and the main indices of the enzymatic (superoxide dismutase, catalase, glutathione reductase, and glutathione peroxidase) and non-enzymatic (reduced glutathione and thioredoxin) antioxidative barrier were assessed. The total oxidative status (TOS) and concentrations of hydrogen peroxide, xanthine oxidase, myeloperoxidase, and oxidized glutathione were measured as markers of oxidative status. The oxidative stress index (OSI) was calculated (TOS/TAS) to estimate the intensity of oxidative stress in the kidney. The exposure to Cd, dose- and duration-dependently, weakened the enzymatic and non-enzymatic antioxidative potential of the kidney leading to a decrease in its TAS, as well as enhanced oxidative status of this organ resulting in the development of oxidative stress. The administration of AM during the low-level and moderate intoxication with Cd significantly protected from this xenobiotic-induced disruption of the oxidative/antioxidative balance and development of oxidative stress in the kidney. In summary, even low-level long-term exposure to Cd may result in the occurrence of oxidative stress in the kidney, whereas supplementation with chokeberry products may improve the oxidative/antioxidative balance preventing oxidative stress in this organ.

The role of oxidized non-coding RNAs of the epigenome in the development of human diseases (literature review)

The attention of scientists to the role of the epigenome in the development of human diseases is associated with the discovery of new non-coding RNA molecules of the epigenome that affect gene expression with changes in protein function and the development of diseases. The study analyzed current scientific data on the effect of oxidative stress induced by cadmium on the regulatory mechanisms of the epigenome, resulting in the development of pathological changes in the body. The results of the study showed that cadmium manifests its toxicity by oxidizing micro RNAs and long RNAs that regulate gene expression without changing DNA/histone complexes. It has been shown that epigenetic disorders under the influence of cadmium-induced oxidative stress can be transmitted to offspring without changing the genotype, and these aberrant changes in non-coding RNA expression patterns are associated with aging, cancer, neurodegenerative, cardiovascular diseases, etc. Circulating micro RNAs that are sensitive to oxidative stress are reported to be potential biomarkers of cardiovascular diseases, including myocardial infarction, hyper­trophy, ischemia/reperfusion, and heart failure. Many studies are aimed at using microRNAs for therapeutic purposes. The complete expression profile of microRNAs in human atherosclerotic plaques was studied, and the mechanisms affecting their formation were identified. Specific microRNAs and reactive oxygen species were identified as potential biomarkers in human malignancies, which expands the possibilities of their use as therapeutic targets. Unlike micro RNAs, the expression of long RNAs has tissue and species specificity, making them important candidates for specific disease markers. The role of these RNAs in carcinogenesis is being actively studied. A large number of them are disrupted at various types of cancer and may play an im­portant role in the onset, metastasis, and therapeutic response of cancer. Thus, oxidative stress induced by cad­mium affects non-coding RNAs, which disrupts the regulatory mechanisms of the epigenome and affects the deve­lopment of cardiovascular, oncological, pulmonary and other human diseases. The search for the impact of non-coding RNAs on the epigenome is constantly growing and has great scientific and practical prospects in medicine.

Selenium alleviates cadmium-induced oxidative stress, endoplasmic reticulum stress, and apoptosis in L8824 cells

Cadmium (Cd) is a toxic pollutant in industrial production that induces organ damage and apoptosis, While, selenium (Se) has the biological function of antagonizing Cd toxicity. Hence, to gain further insight into the protective mechanisms of selenium against Cd-induced damage in Ctenopharyngodon idella liver (L8824) cells, L8824 were exposed to 5 μM, 15 μM, 25 μM cadmium chloride for 24 h after pre-incubation with 25 μM sodium selenite for 9 h. Cell proliferation and morphological changes, the levels of reactive oxygen species (ROS) and antioxidant enzyme activity, mitochondrial membrane potential (MMP), endoplasmic reticulum stress (ERS)-related pathway genes expression, intracellular calcium levels and apoptosis were assessed to explore the protective effect of selenium in Cd-induced L8824 cell damage. The results showed that Cd caused decreased cell viability, ROS accumulation, reduced activity of antioxidant enzymes (SOD, CAT GPx and T-AOC) and apoptosis in L8824 cells. The incubation of Se prominently ameliorated cell proliferation, activated the Keap1-Nrf2 pathway, and restored antioxidant enzyme activity. Furthermore, the expression of grp78, perk, eif-2α, atf4, chop bax, jnk, caspase-3 and caspase-9 was significantly upregulated after Cd exposure, while the expression of bcl-2 was significantly downregulated. Se supplementation alleviated Cd-induced ERS and apoptosis. Moreover, Cd-induced elevation of intracellular Ca2+ levels were alleviated by dantrolene and 2-APB, suggesting that intracellular calcium disorders were caused by Ca2+ released by RyR and IP3R-mediated ER. The results of this study suggested that Cd could induce oxidative stress, ERS, mitochondrial damage and evoke apoptosis, whereas Se had protective effects in preventing Cd induced damage by inhibiting ERS, maintaining intracellular calcium homeostasis, enhancing the antioxidant capacity of L8824 cells and downregulating the Keap1/Nrf2 pathway.

Role of selenium and vitamin E in renal cadmium-induced oxidative stress in rats

Role of selenium and vitamin E in renal cadmium-induced oxidative stress in rats

Evidence of the protective role of D-Aspartate in counteracting/preventing cadmium-induced oxidative stress in the rat testis

Cadmium (Cd), by producing oxidative stress and acting as an endocrine disruptor, is known to cause severe testicular injury, documented by histological and biomolecular alterations, such as decreased serum testosterone (T) level and impairment of spermatogenesis. This is the first report on the potential counteractive/preventive action of D-Aspartate (D-Asp), a well-known stimulator of T biosynthesis and spermatogenesis progression by affecting hypothalamic-pituitary-gonadal axis, in alleviating Cd effects in the rat testis. Our results confirmed that Cd affects testicular activity, as documented by the reduction of serum T concentration and of the protein levels of steroidogenesis (StAR, 3β-HSD, and 17β-HSD) and spermatogenesis (PCNA, p-H3, and SYCP3) markers. Moreover, higher protein levels of cytochrome C and caspase 3, together with the number of cells positive to TUNEL assay, indicated the intensification of the apoptotic process. D-Asp administered either simultaneously to Cd, or for 15 days before the Cd-treatment, reduced the oxidative stress induced by the metal, alleviating the consequent harmful effects. Interestingly, the preventive action of D-Asp was more effective than its counteractive effect. A possible explanation is that giving D-Asp for 15 days induces its significant uptake in the testes, reaching the concentrations necessary for optimum function. In summary, this report highlights, for the first time, the beneficial role played by D-Asp in both counteracting/preventing the adverse Cd effects in the rat testis, strongly encouraging further investigations to consider the potential value of D-Asp also in improving human testicular health and male fertility.

Cadmium-induced oxidative stress responses and acclimation in plants require fine-tuning of redox biology at subcellular level.

Cadmium (Cd) is one of the most toxic compounds released into our environment and is harmful to human health, urging the need to remediate Cd-polluted soils. To this end, it is important to increase our insight into the molecular mechanisms underlying Cd stress responses in plants, ultimately leading to acclimation, and to develop novel strategies for economic validation of these soils. Albeit its non-redox-active nature, Cd causes a cellular oxidative challenge, which is a crucial determinant in the onset of diverse signalling cascades required for long-term acclimation and survival of Cd-exposed plants. Although it is well known that Cd affects reactive oxygen species (ROS) production and scavenging, the contribution of individual organelles to Cd-induced oxidative stress responses is less well studied. Here, we provide an overview of the current information on Cd-induced organellar responses with special attention to redox biology. We propose that an integration of organellar ROS signals with other signalling pathways is essential to finetune plant acclimation to Cd stress.

Potentilla anserina polysaccharide alleviates cadmium-induced oxidative stress and apoptosis of H9c2 cells by regulating the MG53-mediated RISK pathway.

Oxidative stress plays a crucial role in cadmium (Cd)-induced myocardial injury. Mitsugumin 53 (MG53) and its mediated reperfusion injury salvage kinase (RISK) pathway have been demonstrated to be closely related to myocardial oxidative damage. Potentilla anserina L. polysaccharide (PAP) is a polysaccharide with antioxidant capacity, which exerts protective effect on Cd-induced damage. However, it remains unknown whether PAP can prevent and treat Cd-induced cardiomyocyte damages. The present study was desgined to explore the effect of PAP on Cd-induced damage in H9c2 cells based on MG53 and the mediated RISK pathway. For in vitro evaluation, cell viability and apoptosis rate were analyzed by CCK-8 assay and flow cytometry, respectively. Furthermore, oxidative stress was assessed by 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA) staining and using superoxide dismutase (SOD), catalase (CAT), and glutathione/oxidized glutathione (GSH/GSSG) kits. The mitochondrial function was measured by JC-10 staining and ATP detection assay. Western blot was performed to detect the expression of proteins related to MG53, the RISK pathway, and apoptosis. The results indicated that Cd increased the levels of reactive oxygen species (ROS) in H9c2 cells. Cd decreased the activities of SOD and CAT and the ratio of GSH/GSSG, resulting in decreases in cell viability and increases in apoptosis. Interestingly, PAP reversed Cd-induced oxidative stress and cell apoptosis. Meanwhile, Cd reduced the expression of MG53 in H9c2 cells and inhibited the RISK pathway, which was mediated by decreasing the ratio of p-AktSer473/Akt, p-GSK3βSer9/GSK3β and p-ERK1/2/ERK1/2. In addition, Cd impaired mitochondrial function, which involved a reduction in ATP content and mitochondrial membrane potential (MMP), and an increase in the ratio of Bax/Bcl-2, cytoplasmic cytochrome c/mitochondrial cytochrome c, and Cleaved-Caspase 3/Pro-Caspase 3. Importantly, PAP alleviated Cd-induced MG53 reduction, activated the RISK pathway, and reduced mitochondrial damage. Interestingly, knockdown of MG53 or inhibition of the RISK pathway attenuated the protective effect of PAP in Cd-induced H9c2 cells. In sum, PAP reduces Cd-induced damage in H9c2 cells, which is mediated by increasing MG53 expression and activating the RISK pathway.

Insight into the physiological and biochemical mechanisms of biostimulating effect of Ascophyllum nodosum and Moringa oleifera extracts to minimize cadmium-induced oxidative stress in rice.

Cadmium (Cd) is a serious threat for environmental sustainability as it can be taken up quickly by plants and transported to the food chain of living organisms. It alters plants' metabolic and physiological activities and causes yield loss, thereby, enhancing plant tolerance to Cd stress is of utmost essential. Therefore, an experiment was executed to investigate the potential role of Ascophyllum nodosum extract (ANE) and moringa (Moringa oleifera) leaf extract (MLE) to confer Cd tolerance in rice (Oryza sativa cv. BRRI dhan89). Thirty-five-day-old seedling was subjected to Cd stress (50mgkg-1 CdCl2) alone and in a combination of ANE (0.25%) or MLE (0.5%) in a semi-controlled net house. Exposure to Cd resulted in accelerated production of reactive oxygen species, enhanced lipid peroxidation, and disrupted antioxidant defense and glyoxalase system, thus retarded plant growth, biomass production, and yield attributes of rice. On the contrary, the supplementation of ANE or MLE enhanced the contents of ascorbate and glutathione, and the activities of antioxidant enzymes such as ascorbate peroxidase, dehydroascorbate reductase, monodehydroascorbate reductase, glutathione reductase, glutathione peroxidase, and catalase. Moreover, supplementation of ANE and MLE enhanced the activities of glyoxalase I and glyoxalase II which prevented the overgeneration of methylglyoxal in Cd stressed rice plants. Thus, because of ANE and MLE addition Cd-induced rice plants showed a noticeable declination in membrane lipid peroxidation, hydrogen peroxide generation, and electrolyte leakage, whereas improved water balance. Furthermore, the growth and yield attributes of Cd-affected rice plants were improved with the supplementation of ANE and MLE. All the studied parameters indicates the potential role of ANE and MLE in mitigating Cd stress in rice plants through improving the physiological attributes, modulating antioxidant defense and glyoxalase system.