Short-term effects of cadmium exposure on energy reserves and stress markers on Ophelia bicornis Savigny, 1822 (Polychaeta: Opheliidae)

The immunotoxic effects of cadmium (Cd) exposure in bivalves are poorly understood and whether or not stimulation of the immune system exacerbates Cd toxicity is unclear. The mussel Mytilus edulis was exposed to 20 or 50 μg/l total Cd for up to 11 days compared to no added Cd controls to assess immune and other physiological responses. Selected experiments were then repeated in the presence of a lipopolysaccharide (LPS) challenge with and without subsequent Cd exposure. Immune functions of hemocytes, hematology, hemolymph glucose and ion content, as well as superoxide dismutase (SOD) activity and organ pathology were measured. Cd accumulated mainly in digestive gland and gills and to a lesser extent in the adductor muscle. Exposure to 20 μg/l Cd alone caused a transient modulated of phagocytosis and increased neutral red retention (Kruskal-Wallis, p = 0.002). The higher Cd concentration also increased cytotoxicity, and decreased hemocyte count. Changes in hemolymph Na(+), K(+), and glucose were small or negligible. Histopathological examination showed tissue injuries consistent with inflammation and necrosis in the gills, digestive gland, and adductor muscle during Cd exposure alone. LPS injection alone and LPS + Cd caused an increase in the number of circulating hemocytes by the end of the experiment (Kruskal-Wallis, p = 0.01) and a transient rise in phagocytosis at day 4 (analysis of variance (ANOVA), p = 0.001). The LPS + Cd treatment also caused transient changes in neutral red retention and in the cytotoxicity of hemocytes compared to controls. Intracellular SOD activity did not change in hemocytes under any treatment. Tissue inflammation and pathology was greatly increased by the effect of Cd exposure with an LPS injection compared to either treatment alone. We conclude that immunostimulation with LPS can greatly increase Cd-related organ pathologies but does not necessarily alter the responses of hemocytes.

Physiological and biochemical responses of the estuarine pulmonate mud snail, Amphibola crenata, sub-chronically exposed to waterborne cadmium

Cadmium exposure suppresses insulin secretion through mtROS-mediated mitochondrial dysfunction and inflammatory response in pancreatic beta cells

Accumulation and oxidative stress biomarkers in Japanese flounder larvae and juveniles under chronic cadmium exposure

BackgroundChickpea (Cicer arietinum L.), a critical diploid legume in the Fabaceae family, is a rich source of protein, vitamins, and minerals. However, heavy metal toxicity severely affects its growth, yield, and quality. MicroRNAs (miRNAs) play a crucial role in regulating plant responses to both abiotic and biotic stress, including heavy metal exposure, by suppressing the expression of target genes. Plants respond to heavy metal stress through miRNA-mediated regulatory mechanisms at multiple physiological, biochemical, and molecular levels. Although the Fabaceae family is well represented in miRNA studies, chickpeas have been notably underrepresented. This study aimed to investigate the effects of heavy metal-induced stress, particularly from 100 µM concentrations of cadmium (Cd), chromium (Cr), nickel (Ni), lead (Pb), and 30 µM arsenic (As), on two chickpea varieties: ILC 482 (sensitive) and Azkan (tolerant). The assessment focused on physiological, biochemical, and molecular parameters. Furthermore, a systematic characterization of the miR172 gene family in the chickpea genome was conducted to better understand the plant’s molecular response to heavy metal stress.ResultsVariance analysis indicated significant effects of genotype (G), treatment (T), and genotype-by-treatment (GxT) interactions on plant growth, physiological, and biochemical parameters. Heavy metal stress negatively impacted plant growth in chickpea genotypes ILC 482 and Azkan. A reduction in chlorophyll content and relative leaf water content was observed, along with increased cell membrane damage. In ILC 482, the highest hydrogen peroxide (H₂O₂) levels in shoot tissue were recorded under As, Cd, and Ni treatments, while in Azkan, peak levels were observed with Pb treatment. Malondialdehyde (MDA) levels in root tissue were highest in ILC 482 under Cd and Ni exposure and in Azkan under As, Cr, and Cd treatments. Antioxidant enzyme activities, including superoxide dismutase (SOD), catalase (CAT), peroxidase (POD), and ascorbate peroxidase (APX), were significantly elevated under heavy metal stress in both genotypes. Gene expression analysis revealed upregulation of essential antioxidant enzyme genes, such as SOD, CAT, and APX, with APX showing notable increases in both shoot and root tissues compared to the control. Additionally, seven miR172 genes (miR172a, miR172b, miR172c, miR172d, miR172e, miR172f, and miR172g) were identified in the chickpea genome, distributed across five chromosomes. All genes exhibited conserved hairpin structures essential for miRNA functionality. Phylogenetic analysis grouped these miR172 genes into three clades, suggesting strong evolutionary conservation with other plant species. The expression analysis of miR172 and its target genes under heavy metal stress showed varied expression patterns, indicating their role in enhancing heavy metal tolerance in chickpea.ConclusionsHeavy metal stress significantly impaired plant growth and physiological and biochemical parameters in chickpea genotypes, except for cell membrane damage. The findings underscore the critical role of miR172 and its target genes in modulating chickpea’s response to heavy metal stress. These insights provide a foundational understanding for developing stress-tolerant chickpea varieties through miRNA-based genetic engineering approaches.

Glutathione, a tripeptide with sulfhydryl (-SH) group is a very crucial compound primarily involved in redox balance maintenance of the cellular environment. In this study, we monitored the influence of Cd exposure on the transcript levels of glutathione metabolic genes in bud tissues, the youngest leaf, of Camellia sinensis L. In addition, some physiochemical parameters were also studied. Cd exposure decreased chlorophyll and protein contents, while increase was observed in lipid peroxidation upon Cd treatments. These changes were found to be concentration and duration dependent, indicating the occurrence of oxidative stress upon Cd exposure. The transcript levels of glutathione biosynthetic genes viz. gamma-glutamylcysteine synthetase (gamma-ECS) and glutathione synthetase (GSHS) increased upon Cd exposure. Furthermore, transcript levels of glutathione reductase (GR), an enzyme involved in reduction of oxidized glutathione (GSSG) to reduced glutathione (GSH), also showed upregulation on Cd exposure. However, the transcript levels of glutathione-S-transferase (GST), an enzyme involved in forming metal-GSH complex and help in sequestration of high levels of metal ions to vacuole, did not show any change on Cd treatment. This study document that Cd exposure induces oxidative stress in Camellia sinensis and the upregulation in transcript levels of glutathione metabolic genes except GST have suggested the role of these enzymes in the protection of plants from high level Cd exposure.

Are metallothioneins equally good biomarkers of metal and oxidative stress?

Cadmium promoted LPS-induced inflammation through TLR4/IκBα/NFκ-B signaling by increasing ROS-mediated incomplete autophagy

The influence of phosphorus on leaf function, cadmium accumulation and stress tolerance of poplar leaves under cadmium exposure

The effects of cadmium (Cd) and copper (Cu) stress on antioxidant enzyme activities, pigment (total chlorophyll and carotenoid), malondialdehyde (MDA) and total soluble protein contents were determined in Lemna gibba L., Lemna minor L. and Spirodela polyrhiza (L.) Schleid under laboratory conditions. Cd and Cu were separately applied at concentrations of 0.01, 0.05, 0.1, 0.5 and 1.5 mg L-1 for 96 hours. The results of this study showed that Cd and Cu affected the physiological status of L. gibba, L. minor and S. polyrhiza. Decreased total chlorophyll and increased total soluble protein contents were evident in S. polyrhiza under Cu and Cd exposure. Cd treatment caused increased MDA contents in L. minor (0.5 and 1.5 mg L-1) and S. polyrhiza (0.5 mg L-1), while exposure to Cu caused an increase only in S. polyrhiza (0.05 and 0.1 mg L-1). Catalase (CAT) activity showed increases only in L. minor under Cd and Cu treatment. For ascorbate peroxidase (APX) activity, significant effects of Cu and Cd were determined in L. gibba. However, no significant changes were observed in L. minor treated with Cu and Cd (except for at 1.5 mg L-1). APX activity started to increase at 0.5 mg L-1 Cd in S. polyrhiza. Guaiacol peroxidase (POD) activity significantly increased in all plants (with a few exceptions in S. polyrhiza) under Cd and Cu exposure. According to principal component analysis, the three plant species were separated from each other on the basis of activities of antioxidant enzymes (L. gibba), pigment contents (L. minor), MDA and soluble protein contents (S. polyrhiza).

Cadmium (Cd) is a highly toxic heavy metal that can be found everywhere in the environment and can have harmful effects on both human and animal health. Pinostrobin (PSB) is a bioactive natural flavonoid isolated from Boesenbergia rotunda with several pharmacological properties, such as antiinflammatory, anticancer, antioxidant, and antiviral. This investigation was intended to assess the therapeutic potential of PSB against Cd-induced kidney damage in rats. In total, 48 Sprague Dawley rats were divided into four groups: a control, a Cd (5 mg/kg), a Cd + PSB group (5 mg/kg Cd and 10 mg/kg PSB), and a PSB group (10 mg/kg) that received supplementation for 30 days. Exposure to Cd led to a decrease in the activities of catalase (CAT), glutathione reductase (GSR), superoxide dismutase (SOD), and glutathione peroxidase (GSH-PX), whereas levels of reactive oxygen species (ROS) and malondialdehyde (MDA) increased. Cd exposure also caused a substantial increase in urea, kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), and creatinine levels. Moreover, a noticeable decline was noticed in creatinine clearance. Moreover, Cd exposure considerably increased the levels of inflammatory indices, including interleukin-1b (IL-1b), tumor necrosis factor-a (TNF-a), interleukin-6 (IL-6), nuclear factor kappa-B (NF-kB), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) activity. Cd treatment decreased the expression of the antiapoptotic markers (Bcl-2) while increasing the expression of apoptotic markers (Bax and Caspase-3). Furthermore, Cd treatment substantially reduced the TCA cycle enzyme activity, such as alpha-ketoglutarate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, and isocitrate dehydrogenase. Moreover, mitochondrial electron transport chain enzymes, succinatedehydrogenase, NADH dehydrogenase, cytochrome c-oxidase, and coenzyme Q-cytochrome reductase activities were also decreased following Cd exposure. PSB administration substantially reduced the mitochondrial membrane potential while inducing significant histological damage. However, PSB treatment significantly reduced Cd-mediated renal damage in rats. Thus, the present investigation discovered that PSB has ameliorative potential against Cd-induced renal dysfunction in rats.

The effects of 60-d cadmium (Cd) exposure on enzymatic and non-enzymatic antioxidative system of Oryza sativa L. seedlings at tillering stage were studied using soil culture experiment. Research findings showed that chlorophyll content of Oryza sativa L. declined with the increase in soil metal concentration. Cd pollution induced the antioxidant stress by inducing O2 −1 and H2O2, which increased in plants; at the same time, MDA as the final product of peroxidation of membrane lipids, accumulated in plant. The antioxidant enzyme system was initiated under the Cd exposure, i.e. almost all the activities of superoxide dismutase (SOD), peroxidase, catalase, glutathione peroxidase, and ascorbate peroxidase were elevated both in leaves and roots. The non-protein thiols including phytochelatins and glutathione to scavenge toxic free radicals caused by Cd stress was also studied. The contents of phytochelatins and glutathione were about 3.12–6.65-fold and 3.27–10.73-fold in leaves, against control; and the corresponding values were about 3.53–9.37-fold and 1.41–5.11-fold in roots, accordingly.

Histopathological and biochemical alternations of the heart induced by acute cadmium exposure in the freshwater crab Sinopotamon yangtsekiense

Cadmium (Cd) exposure through Hyphantria cunea pupae reduces the parasitic fitness of Chouioia cunea: A potential risk to its biocontrol efficiency

The aim of this study was to investigate the hemodynamic, oxidative stress (OS), and nitric oxide (NO) responses to a submaximal isometric exercise session (IES) involving large muscle mass. Fourteen hypertensive (HTG: age = 35.9 ± 8.1 yr, height = 1.73 ± 0.10 m, total body mass = 78.0 ± 15.8 kg) and 10 normotensive (NTG: age = 41.1 ± 9.4 yr, height = 1.71 ± 0.12 m, total body mass = 82.3 ± 22.4 kg) participants performed two experimental sessions in the leg press and bench press: (i) control session and (ii) 8 sets × 1 min contraction at 30% maximal voluntary isometric contraction with 2-min rest interval. Blood pressure (BP) was measured at rest and during 60 min postexercise. Blood samples were collected at rest, immediately after the session, and 60 min postexercise. NO was obtained through the Griess reaction method. OS parameters were analyzed using commercial kits. A repeated-measures ANOVA with Bonferroni post hoc test was used to analyze all dependent variables. A significant decrease in systolic BP was observed only for HTG at 45 and 60 min postexercise (baseline vs 45 min: P = 0.03, Δ% = 4.44%; vs 60 min: P = 0.018, Δ% = 5.58%). NO increased immediately postexercise only for HTG (P = 0.008, Δ% = 16.44%). Regarding OS parameters, thiobarbituric acid reactive substances presented a significant reduction 60 min after the IES for NTG and HTG; catalase increased in both groups. The data showed that only 8 min of IES with a large muscle mass elicits an elevated pro-oxidant activity leading to a greater NO bioavailability, increases antioxidant reaction, and consequently reduces BP in hypertensive patients.