Effects of microbeads and cadmium on oxidative stress and apoptosis in rockfish Sebastes schlegeli: comparison of single and combined environmental conditions

Micro plastics (MPs) have gained attention as new pollutants worldwide, but little is known about how it interacts with metal contamination in soil-plant ecosystems. Here, research looked into how Cadmium (Cd) and Micro plastics, such as polyethylene (PE) and polylactic acid (PLA), affected the growth of plants and the neighborhood of arbuscular mycorrhizal fungi in agricultural Soil. While 10% PLA reduced the total biomass of maize and the amount of chlorophyll in the leaves, PE showed no discernible phytotoxicity. Between PE and Cadmium, there was an important impact on the volume of roots, but likewise, PLA nor Cadmium had an important effect. PE and PLA showed minimal impact on cadmium accumulation in plant tissues, but they increased soil pH and DTPA-extractable cadmium concentrations. Different treatments showed different counts of pandemic and total OTUs. Arbuscular mycorrhizal fungus (AMF) taxa showed a highly variable abundance ratio with Micro plastics and Cadmium. According to the type and dose of Micro plastics, AMF diversity in communities and structure was changed. The dominant AMF genus exhibited but significant interactions with Micro plastics which were further influenced by the presence of Cadmium. Overall, MP sort and quantity, Cadmium and the way it interacts, and the high dose of PLA induced increased phytotoxicity, which changed with the growth of plants and the AMF. In conclusion, coexisting Micro plastics and Cadmium could collectively influence plant function and root symbiosis changes, increasing the dangers to agriculture systems and habitat biodiversity.

Inhibition of DNA mismatch repair by cadmium and oxidative damage

The objective of the present work was to evaluate the effect of exogenously applied cadmium on the physiological response of green algae Chlorella vulgaris. The study investigated the long-term effect (18 days) of cadmium on the levels of algae biomass, assimilation pigment composition, soluble protein, oxidative status (production of hydrogen peroxide and superoxide anion), antioxidant enzymes (such as superoxide dismutase, peroxidase, catalase and glutathione reductase enzyme) in C. vulgaris. The results showed that growth, the amount of chlorophyll a (Chl a), chlorophyll b (Chl b) and carotenoids gradually decreased with increasing cadmium over 18 days exposure. Cadmium at concentration of 7 mg L−1 inhibited algal growth expressed as the number of cells. Our research found that C. vulgaris has a high tolerance to cadmium. Contents of chlorophylls (Chl a and Chl b) and carotenoids (Car) of C. vulgaris was significantly decline with rising concentration of cadmium (p < 0.05). The decrease of 54.04 and 93.37 % in Chl a, 60.65 and 74.32 % in Chl b, 50.00 and 71.88 % in total carotenoids was noticed following the treatment with 3 and 7 mg L−1 cadmium doses compared with control treatment, respectively. Cadmium treatments caused a significant change in the physiological competence (calculated as chlorophyll a/b) which increased with increasing Cd(II) doses up to 1 mg L−1 but decreased at 3 mg L−1. While accumulation of soluble protein was enhanced by presence of cadmium, the treatment with cadmium at 3 and 7 mg L−1 increased the concentration of soluble proteins by 88, 95.8 % in C. vulgaris, respectively. Moreover, low doses of cadmium stimulated enzymatic (superoxide dismutase, catalase and glutathione reductase) in C. vulgaris, The content of peroxidase increased with the increasing cadmium concentration, and had slightly decreased at the concentration of 7 mg L−1, but was still higher than control group, which showed that cadmium stress at high concentration mainly peroxidase works in C. vulgaris. And therefore, suppressed reactive oxygen species (hydrogen peroxide and superoxide) accumulated. The present study also showed that cadmium increased oxidative stress and induced antioxidant defense systems against reactive oxygen species. The observation in here analyzed C. vulgaris after exposure to cadmium indicate that hydrogen peroxide, superoxide and peroxidase in the alga with exposure to Cd(II) seemed to be parameters as biomarkers for metal-induced oxidative stress.

Effects of waterborne cadmium on metabolic rate, oxidative stress, and ion regulation in the freshwater fish, inanga (Galaxias maculatus)

BackgroundSoils contaminated with heavy metals (HMs) pose a risk to human health via the food chain, as many edible plants absorb these metals. In turn, some of these plants could be used as phytoremediators for such soils. Calligonum comosum is an indigenous medicinal shrub that grows naturally in wide swaths of sandy soil in Saudi Arabia and has many advantages that render it a promising candidate for the treatment of HM-contaminated areas. But the impact of HM on this plant remains unknown, especially in the early stages of its development.ObjectiveThis investigation aimed to study the effects of lead (Pb) and cadmium (Cd) on the germination of C. comosum seeds under laboratory conditions, and assess the seeds’ response to these metals.MethodsThe C. comosum seed germination was monitored in Petri dishes containing Pb and Cd at increasing concentrations (25, 50, 75, and 100 µM) for up to 3 weeks. SDS-PAGE was used to examine the protein profile of germinated seeds and the western blot was used to assess the influence of HMs on the activities of the catalase enzyme and the beta subunit of ATP synthase (AtpB).ResultsThe germination rate and speed of C. comosum seeds were delayed by increasing concentrations of either Pb or Cd, but this effect was dose-dependent. SDS-PAGE analysis results revealed that exposure to both metals led to altered protein profiles as indicated by the resulting band intensities and disappearance of some proteins compared with the untreated controls. Further, the western blot analysis detected greater activity of catalase enzyme as well as AtpB in the Cd- and Pb-treated seeds.ConclusionC. comosum seeds treated with Cd or Pb enhance protein degradation and denaturation beside oxidative stress, leading to reduced seed viability. These results suggest oxidoreduction proteins and those involved in ATP synthesis are enhanced in C. comosum seeds in response to Cd and Pb stressors, which is a probable mechanism by which seeds may tolerate heavy metal stress.

Cadmium, as a hazardous pollutant commonly present in the living environment, represents an important risk to human health due to its undesirable effects (oxidative stress, changes in activities of many enzymes, interactions with biomolecules including DNA and RNA) and consequent potential risk, making its detection very important. New and unique technological and biotechnological approaches for solving this problems are intensely sought. In this study, we used the commonly occurring potential pathogenic microorganism Staphylococcus aureus for the determination of markers which could be used for sensing of cadmium(II) ions. We were focused on monitoring the effects of different cadmium(II) ion concentrations (0, 1.25, 2.5, 5, 10, 15, 25 and 50 μg mL−1) on the growth and energetic metabolism of Staphylococcus aureus. Highly significant changes have been detected in the metabolism of thiol compounds—specifically the protein metallothionein (0.79–26.82 mmol/mg of protein), the enzyme glutathione S-transferase (190–5,827 μmol/min/mg of protein), and sulfhydryl groups (9.6–274.3 μmol cysteine/mg of protein). The ratio of reduced and oxidized glutathione indicated marked oxidative stress. In addition, dramatic changes in urease activity, which is connected with resistance of bacteria, were determined. Further, the effects of cadmium(II) ions on the metabolic pathways of arginine, β-glucosidase, phosphatase, N-acetyl β-d-glucosamine, sucrose, trehalose, mannitol, maltose, lactose, fructose and total proteins were demonstrated. A metabolomic profile of Staphylococcus aureus under cadmium(II) ion treatment conditions was completed seeking data about the possibility of cadmium(II) ion accumulation in cells. The results demonstrate potential in the application of microorganisms as modern biosensor systems based on biological components.

Worldwide actions against plastic pollution from microbeads and microplastics in cosmetics focusing on European policies. Has the issue been handled effectively?

Cadmium triggers apoptosis of LLC-PK1 cells through induction of endoplasmic reticulum (ER) stress. We found that cadmium caused generation of reactive oxygen species (ROS) and that cadmium-induced ER stress was inhibited by antioxidants. In contrast, suppression of ER stress did not attenuate cadmium-triggered oxidative stress, suggesting that ER stress occurs downstream of oxidative stress. Exposure of the cells to either O(2)(*), H(2)O(2), or ONOO(-) caused apoptosis, whereas ER stress was induced only by O(2)(*) or ONOO(-). Transfection with manganese superoxide dismutase significantly attenuated cadmium-induced ER stress and apoptosis, whereas pharmacological inhibition of ONOO(-) was ineffective. Interestingly, transfection with catalase attenuated cadmium-induced apoptosis without affecting the level of ER stress. O(2)(*) caused activation of the activating transcription factor 6-CCAAT/enhancer-binding protein-homologous protein (CHOP) and the inositol-requiring ER-to-nucleus signal kinase 1-X-box-binding protein 1 (XBP1) proapoptotic cascades, and overexpression of manganese superoxide dismutase attenuated cadmium-triggered induction of both pathways. Furthermore, phosphorylation of proapoptotic c-Jun N-terminal kinase by O(2)(*) or cadmium was suppressed by dominant-negative inhibition of XBP1. These data elucidated 1) cadmium caused ER stress via generation of ROS, 2) O(2)(*) was selectively involved in cadmium-triggered, ER stress-mediated apoptosis through activation of the activating transcription factor 6-CHOP and inositol-requiring ER-to-nucleus signal kinase 1-XBP1 pathways, and 3) phosphorylation of JNK was caused by O(2)(*)-triggered activation of XBP1.

Increasing intracellular cAMP and cGMP inhibits cadmium-induced oxidative stress in rat submandibular saliva

Heavy metal poisoning can have serious health consequences, including damage to the brain, kidneys, and other organs. Cadmium is a toxic heavy metal that can accumulate in the body over time and the exposure to this element has been linked to a variety of adverse health effects. Cadmium toxicity can lead to an imbalance in the cellular redox state and be a source of oxidative stress. On the molecular level, cadmium ions negatively affect cellular metabolism, including the disruption of energy production, protein synthesis, and DNA damage. The study has been carried out on a group of 140 school-age children (8 to 14 years old) inhabiting the industrialized areas of Upper Silesia. The study population was divided into two sub-groups based on the median concentration of cadmium in blood (0.27 µg/L): Low-CdB and High-CdB. Measured traits comprised blood cadmium levels (CdB) as well as a blood count and selected oxidative stress markers. This research study aimed to demonstrate a correlation between the impact of exposure to elevated cadmium concentrations in a population of children and certain markers of oxidative stress, and 25-OH vitamin D3 concentration. A negative correlation has been found between cadmium concentration and 25-OH vitamin D3 level, protein sulfhydryl groups content in blood serum, glutathione reductase activity, and lipofuscin and malondialdehyde levels in erythrocytes. The concentration of 25-OH vitamin D3 in the High-CdB group was decreased by 23%. The oxidative stress indices can be considered a valuable indicator of early Cd-toxicity effects to be included in the routinely-applied cadmium exposure monitoring parameters, allowing the evaluation of stress intensity to the cell metabolism.

Leaves of two-week old seedlings of tomato (Lycopersicon esculentum) were treated with various concentrations (0∼100 M) of <TEX>$CdCl_2$</TEX> for up to 9 days and subsequent growth of seedlings, symptoms of oxidative stress and isozyme activities of antioxidant enzymes including superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX) and peroxidase (POX) were investigated. Compared with the non-treated control, Cd exposure decreased biomass but increased Cd accumulation, hydrogen peroxide production and lipid peroxidation as malondialdehyde (MDA) formation in leaves and roots. Further studies on the developmental changes of isozyme activities showed that Fe-SOD, Cu/Zn-SOD and one of three APX isozymes decreased and CAT and one of four POX isozymes increased in leaves, whereas Fe-SOD, one of three POX isozymes and two of four APX isozymes decreased and CAT increased in roots, showing different expression of isozymes in leaves and roots with Cd exposure level and time. Based on our results, we suggest that the reduction of seedling growth by Cd exposure is the oxidative stress resulting from the over production of <TEX>$H_2O_2$</TEX> and the insufficient activities of antioxidant enzymes particularly involved in the scavenging of <TEX>$H_2O_2$</TEX>. Further, the decreased activities of SOD and APX isozymes of chloroplast origin, the increased activities of CAT and POX and high <TEX>$H_2O_2$</TEX> contents with Cd exposure might indicate that Cd-induced oxidative stress starts outside chloroplast.

In this study, was investigate the ability of Ginger to adversely histological and physiology effect of cadmium in the liver tissue of rabbit, Ginger is source of antioxidants was administered orally to prevent the adverse effects of cadmium (cd). Twenty four male rabbits were randomized into 3 groups (n = 8), were used for this study. Animals in group (1) served as the control and were drinking distilled water. Animals in groups (2) were drinking2% cadmium chloride. Group (3) animals were, in addition to drinking cadmium, treated with 250 mg/kg of ginger. All treatments were for 12 weeks. The results showed that cadmium caused a significant (p&lt;0.05) reduction in plasma superoxide dismutase and catalase activity, but a significant increase (p&lt;0.05) in plasma malondialdehyde concentration with histological changes in liver cell such as necrosis, hemorrhage with aggregation of some toxic spot as (black spot),protein cast with epithelial cell in group 3 comparison with control and other group , using ginger cause to modified these harmful effects. These findings lead to the conclusion that ginger significantly decreased (p&lt;0.05) the adverse toxic harmful effects of cadmium exposure on the liver as oxidative stress.

Cadmium is a common transition metal that entails an extremely wide range of toxic effects in humans and animals. The cytotoxicity of cadmium ions and its compounds is due to various genotoxic effects, including both DNA damage and chromosomal aberrations. Some bone diseases, kidney and digestive system diseases are determined as pathologies that are closely associated with cadmium intoxication. In addition, cadmium is included in the list of carcinogens because of its ability to initiate the development of tumors of several forms of cancer under conditions of chronic or acute intoxication. Despite many studies of the effects of cadmium in animal models and cohorts of patients, in which cadmium effects has occurred, its molecular mechanisms of action are not fully understood. The genotoxic effects of cadmium and the induction of programmed cell death have attracted the attention of researchers in the last decade. In recent years, the results obtained for in vivo and in vitro experimental models have shown extremely high cytotoxicity of sublethal concentrations of cadmium and its compounds in various tissues. One of the most studied causes of cadmium cytotoxicity is the development of oxidative stress and associated oxidative damage to macromolecules of lipids, proteins and nucleic acids. Brain cells are most sensitive to oxidative damage and can be a critical target of cadmium cytotoxicity. Thus, oxidative damage caused by cadmium can initiate genotoxicity, programmed cell death and inhibit their viability in the human and animal brains. To test our hypothesis, cadmium cytotoxicity was assessed in vivo in U251 glioma cells through viability determinants and markers of oxidative stress and apoptosis. The result of the cell viability analysis showed the dose-dependent action of cadmium chloride in glioma cells, as well as the generation of oxidative stress (p &lt;0.05). Calculated for 48 hours of exposure, the LD50 was 3.1 μg×ml-1. The rates of apoptotic death of glioma cells also progressively increased depending on the dose of cadmium ions. A high correlation between cadmium concentration and apoptotic response (p &lt;0.01) was found for cells exposed to 3–4 μg×ml-1 cadmium chloride. Moreover, a significant correlation was found between oxidative stress (lipid peroxidation) and induction of apoptosis. The results indicate a strong relationship between the generation of oxidative damage by macromolecules and the initiation of programmed cell death in glial cells under conditions of low doses of cadmium chloride. The presented results show that cadmium ions can induce oxidative damage in brain cells and inhibit their viability through the induction of programmed death. Such effects of cadmium intoxication can be considered as a model of the impact of heavy metal pollution on vertebrates.

The effects of cadmium on performance, antioxidant defense system, liver and kidney functions, and cadmium accumulation in selected tissues of broiler chickens were studied. Whether the possible adverse effects of cadmium would reverse with the antioxidant ascorbic acid was also investigated. Hence, 4 treatment groups (3 replicates of 10 chicks each) were designed in the study: control, ascorbic acid, cadmium, and cadmium plus ascorbic acid. Cadmium was given via the drinking water at a concentration of 25 mg/L for 6 wk. Ascorbic acid was added to the basal diet at 200 mg/kg either alone or with cadmium. Cadmium decreased the body weight (BW), body weight gain (BWG), and feed efficiency (FE) significantly at the end of the experiment, whereas its effect on feed consumption (FC) was not significant. Cadmium increased the plasma malondialdehyde (MDA) level as an indicator of lipid peroxidation and lowered the activity of blood superoxide dismutase (SOD). Liver function enzymes, aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and gamma glutamyl transferase (GGT) activities were not changed by cadmium. Cadmium ingestion did not alter serum creatinine levels. Although the serum cadmium level was not elevated, cadmium mainly accumulated in the kidneys, liver, pancreas, and muscle. Ascorbic acid supplementation resulted in a reduction of MDA level previously increased by cadmium and a restoration in SOD activity. However, ascorbic acid did not ameliorate the growth inhibitory effect of cadmium nor did it prevent accumulation of cadmium in analyzed tissues. These data indicate that oxidative stress, induced by cadmium, plays a role in decreasing the performance of broilers and that dietary supplementation by ascorbic acid might be useful in reversing the lipid peroxidation induced by cadmium and partly alleviating the adverse effect of cadmium on performance of broilers.

Effects of cadmium on antioxidant and non-specific immunity of Macrobrachium nipponense