A suspected case of "itai-itai disease" in a cadmium-polluted area in Akita prefecture, Japan.

BACKGROUND: Itai-itai disease is the most severe case of chronic cadmium (Cd) toxicity, which was endemic in Cd-polluted areas in the Jinzu River basin in Toyama prefecture, Japan. Akita prefecture also has Cd-polluted areas, but there have been no cases of "itai-itai disease". CASE PRESENTATION: An elderly female farmer with Cd nephropathy residing in a Cd-polluted area in the northern part of the Akita prefecture was identified through hospital-based screening at Akita Rosai Hospital in Odate city. She had chronic renal failure with a high Cd exposure level and advanced renal tubular dysfunction. The shortening of height, bone deformities and fractures, abnormal bone metabolism suggesting osteomalacia, and renal anemia were also noted. Therefore, "itai-itai disease", similar to cases in the Jinzu River basin, was suspected. CONCLUSION: This is the first case of "itai-itai disease" in a Cd-polluted area in Akita prefecture.

Low-level, chronic ingestion of lead and cadmium: The unspoken danger for at-risk populations.

The long-term effects of low-level, chronic exposure to lead and cadmium through ingestion are often overlooked, despite the urgency surrounding the clinical onset and worsening of certain pathologies caused by these metals. This work reviews current legislation, global ingestion levels, and blood levels in the general population to emphasize the need for reactivity towards this exposure, especially in at-risk populations, including patients with early-stage renal and chronic kidney disease. Global data indicates persistent chronic ingestion of lead and cadmium, with no decreasing trend in recent years, and a daily consumption of tens of micrograms worldwide. Moreover, the average blood lead and cadmium levels in the general population are concerning in many countries with some significantly exceeding healthy limits, particularly for children. Technologies developed to cleanse soil and prevent heavy metal contamination in food are not yet applicable on a global scale and remain financially inaccessible for many communities. Addressing this chronic ingestion at the human level may prove more beneficial in delaying the onset of associated clinical pathologies or preventing them all together.

Cadmium as a male reproductive toxicant and natural and non-natural ways to tackle it: a review.

Cadmium (Cd) is a naturally occurring environmental pollutant, a toxic substance that causes oxidative stress. According to epidemiological studies, the data suggested that environmental and occupational Cd exposure may be related to several diseases and severe testicular damage. However, studies are going on to explore the mechanism of Cd-induced male reproductive toxicity and its treatment strategies. Currently, researchers are focusing on naturally occurring bioactive compounds, plant extracts, and biochemical, which have better efficacy, less toxicity, and high bioavailability. This review focuses on the mechanistic effect of Cd on testicular toxicity and different categories of compounds having a beneficial impact on Cd-induced male reproductive toxicity. Some potent bioactive antioxidants are quercetin, caffeic acid phenethyl ester, cyanidin-3-O-glucoside, curcumin, and silymarin. In comparison, plant extracts are Costus afer leaf methanol extract, methanol root extract of Carpolobia lutea, red carrot methanolic extract, Panax ginseng extract, and biochemicals including melatonin, progesterone, glutamine, L-carnitine, and selenium. Advanced and more detailed studies are needed on these compounds to explore their mechanism in attenuating Cd-induced testicular toxicity and can be potential therapeutics in the future.

Integrated ultrastructural, physiological, transcriptomic, and metabolomic analysis uncovers the mechanisms by which nicotinamide alleviates cadmium toxicity in Pistia stratiotes L.

Exogenous nicotinamide (NIC) is a promising solution to relieve heavy metal (HM) toxicity in plants. Nonetheless, the underlying mechanisms involved remain poorly understood. As NIC addition (200 µM) can increase the tolerance of Pistia stratiotes L. to Cd stress (10 mg L-1), this strategy was subjected to integrated ultrastructural, physiological, transcriptomic, and metabolomic analysis to reveal the mechanisms involved. Exogenous NIC initiated a series of physiological, transcriptional, and metabolic responses that alleviated Cd damage. NIC addition improved Cd transfer from roots to leaves and reduced Cd damage in roots. The transported Cd to leaves did not induce further toxicity because it was abundantly compartmentalised in cell walls, which might be mediated by lignin synthesis. Moreover, NIC addition improved the repair of photosystem II in leaves under Cd stress by inducing key genes (e.g., chlorophyll A-B binding protein and PSII repair protein encoding genes), resulting in the restoration of Fv/Fm. In addition, antioxidant enzyme activities (e.g., peroxidase and catalase) and synthesis of antioxidants (e.g., stachydrine and curculigoside) were triggered to overcome oxidative stress. Our work paves the way for a deeper understanding of the mechanisms by which NIC alleviates HM toxicity in plants, providing a basis for improving phytoremediation.

Reversal Effects of Royal Jelly and Propolis Against Cadmium-Induced Hepatorenal Toxicity in Rats.

Heavy metal toxicity is an exponentially growing health problem. In this study, we aimed to assess the protective properties of propolis and royal jelly against cadmium adverse effects. Thirty-two adult male rats were included in our study; kidney and liver functions, histopathological changes, and the level of oxidative stress were evaluated in rats exposed to a daily dose of 4.5 mg cadmium per kilogram of body weight for 1 month and those cotreated simultaneously with either propolis (50 mg/kg/day) or royal jelly (200 mg/kg/day) with cadmium compared to control animals. Cadmium-mediated hepatorenal toxicity was manifested as per the increased oxidative stress, function deterioration, and characteristic histopathological aberrations. The supplementation of royal jelly or propolis restores most of the affected parameters to a level similar to the control group. However, the parameters describing the grade of DNA damage and the interleukin-1ß expression in the liver, as well as the levels of malondialdehyde and metallothionein, were slightly elevated compared to controls, despite the regular use of royal jelly or propolis. It is worth noting that better results were found in the case of royal jelly compared to propolis administration. Most likely, the ability of both products to chelate cadmium and contribute in reducing oxidative stress is of great importance. However, further investigations are needed to complement the knowledge about the expected nutritional and medicinal values.

Do Nanoparticles of Calcium Disodium EDTA Minimize the Toxic Effects of Cadmium in Female Rats?

The present study aims to investigate the ability of CaNa2EDTA (ethylenediaminetetraacetic acid) macroparticles and nanoparticles to treat cadmium-induced toxicity in female rats and to compare their efficacies. Forty rats were divided into 4 equal groups: control, cadmium, cadmium + CaNa2EDTA macroparticles and Cd + CaNa2EDTA nanoparticles. Cadmium was added to the drinking water in a concentration of 30 ppm for 10 weeks. CaNa2EDTA macroparticles and nanoparticles (50 mg/kg) were intraperitoneally injected during the last 4 weeks of the exposure period. Every two weeks, blood and urine samples were collected for determination of urea, creatinine, metallothionein and cadmium concentrations. At the end of the experiment, the skeleton of rats was examined by X-ray and tissue samples from the kidney and femur bone were collected and subjected to histopathological examination. Exposure to cadmium increased the concentrations of urea and creatinine in the serum and the concentrations of metallothionein and cadmium in serum and urine of rats. A decrease in bone mineralization by X-ray examination in addition to various histopathological alterations in the kidney and femur bone of Cd-intoxicated rats were also observed. Treatment with both CaNa2EDTA macroparticles and nanoparticles ameliorated the toxic effects induced by cadmium on the kidney and bone. However, CaNa2EDTA nanoparticles showed a superior efficacy compared to the macroparticles and therefore can be used as an effective chelating antidote for treatment of cadmium toxicity.

Protective effect of quercetin on cadmium-induced kidney apoptosis in rats based on PERK signaling pathway.

BACKGROUND: Cadmium (Cd) is a highly toxic environmental pollutant that can enter the body through bioaccumulation. The kidney is an important target organ for Cd poisoning. Quercetin (Que) is a natural flavonoid compound with free radical scavenging and antioxidant properties. Previous studies showed that Que can alleviate kidney damage caused by Cd poisoning in rats, but the specific mechanism is still unclear. METHODS: Twenty-four male Sprague-Dawley (SD) rats were divided into four groups: normal saline-treated control group, Cd group treated by intraperitoneal injection of 2 mg/kg b.w. CdCl2, Cd + Que group treated by intraperitoneal injection of 2 mg/kg b.w. CdCl2 and 100 mg/kg b.w. Que, and Que group treated by 100 mg/kg b.w. Que. Four weeks later, the rats were anesthetized with diethyl ether, and blood was taken intravenously. The rats were executed with their necks cut off, and the kidneys were removed. Body weight, kidney organ weight, and glutathione (GSH) and malondialdehyde (MDA) levels were measured. The structure of kidney tissue was observed by hematoxylin and eosin staining, kidney cell apoptosis was detected by TUNEL assay, and the mRNA expression levels of genes related to the PERK signaling pathway were analyzed by RT-PCR. RESULTS: Compared with the control group, the Cd-treated group exhibited a significant decrease in body weight (P < 0.01). Their kidneys showed a significant increase in the relative organ weight (P < 0.01). Moreover, the MDA and GSH levels increased. Kidney tissue damage and renal cell apoptosis were observed, and the mRNA expression levels of genes related to the PERK signaling pathway significantly increased (P < 0.01). Compared with the Cd-treated group, the Cd + Que group exhibited a significant increase in body weight (P < 0.01) and significant decreases in the relative organ weight, MDA and GSH levels, and mRNA expression levels of genes related to the PERK signaling pathway (P < 0.01). Furthermore, kidney tissue damage and renal cell apoptosis were observed. CONCLUSION: Cd treatment resulted in rat weight loss, renal edema, and oxidative stress and caused renal tissue damage and cell apoptosis by activating the PERK signaling pathway. Que was able to restore the body weight and renal coefficient of rats. It also alleviated the oxidative stress and kidney tissue damage caused by Cd and the cell apoptosis caused by Cd through inhibiting the PERK signaling pathway. Thus, Que could be considered for the treatment of kidney diseases caused by Cd poisoning.

Cadmium as an ovarian toxicant: A review.

Cadmium (Cd) is a ubiquitous heavy metal toxicant with no biological function in the human body. Considerably, because of its long biological half-life and very low excretion rate, Cd is inclined to accumulate and cause deleterious effects on various body organs (e.g., liver, kidney, and ovary) in humans and animals. Ovaries are the most vulnerable targets of Cd toxicity. Cd has been shown to induce oxidative stress, follicular atresia, hormonal imbalance, and impairment of oocyte growth and development. Moreover, Cd toxicity has been associated with increasing incidences of menstrual disorders, pregnancy loss, preterm births, delayed puberty, and female infertility. Therefore, it is crucial to understand how Cd poisoning impacts specific ovarian processes for the development of preventive interventions to enhance female fertility. The current review attempts to collate the recent findings on Cd-induced oxidative stress, follicular apoptosis, steroid synthesis inhibition, and teratogenic toxicity, along with their possible mechanisms in the ovarian tissue of different animal species. Additionally, the review also summarizes the studies related to the use of many antioxidants, medicinal herbs, and other compounds as remedial approaches for managing Cd-induced ovarian toxicity.

Epigallocatechin-3-Gallate Reduces Cd-Induced Developmental Toxicity of Bodysize in Caenorhabditis elegans via the PEK-1/eIF-2α/ATF-4 Pathway.

Cadmium (Cd), a harmful heavy metal that has no biological purpose, can harm healthy fetal and child development. Epigallocatechin-3-gallate (EGCG), the most abundant polyphenol in tea, has been shown to increase cell viability under Cd exposure and ameliorate Cd-induced kidney injury in adult male rats. Using the Caenorhabditis elegans (C. elegans) model, we demonstrated that EGCG mitigated Cd-induced body size developmental toxicity through a mechanism that did not involve chelation with EGCG and was not associated with Cd accumulation and efflux. Our research indicated that the beneficial effects of EGCG on Cd-induced body size developmental toxicity were associated with the mitigation of endoplasmic reticulum stress. Furthermore, our observations indicate that EGCG reduced Cd-induced developmental toxicity in C. elegans via the PEK-1/eIF-2α/ATF-4 pathway. Our results provide important evidence for the potential benefits of consuming tea as a detoxification agent.

Cadmium body burden and health effects after restoration of cadmium-polluted soils in cadmium-polluted areas in the Jinzu River basin.

BACKGROUND: Itai-itai disease is caused by environmental cadmium (Cd) pollution in the Jinzu River basin in Japan. To reduce the Cd contamination of rice, soil restoration of paddy fields was carried out. We evaluated the effect of soil restoration on the health status of residents of the former Cd-polluted area. METHODS: Participants were 1,030 men and 944 women who lived in the area of restoration of Cd-polluted rice paddies. First morning urine was collected and urinary Cd, ß2-microglobulin (ß2MG), and N-acetyl-ß-D-glucosaminidase (NAG) levels were measured. Associations among age, years of residence before and after soil restoration, and urinary Cd, ß2MG, and NAG levels were evaluated by multiple regression analysis. RESULTS: The geometric mean (interquartile range) of urinary Cd (µg/g Cr) was 1.00 (0.58-1.68) in men and 1.67 (1.02-2.91) in women. The geometric means of urinary ß2MG (µg/g Cr) and NAG (U/g Cr) were 174.6 (92.6-234.2) and 1.47 (0.72-3.14) in men, and 217.6 (115.3-28.7) and 1.48 (0.73-2.96) in women, respectively. Urinary Cd, ß2MG, and NAG were significantly positively correlated (p < 0.01 all). Age and duration of residence in the Cd-polluted area before soil restoration were independently associated with urinary Cd, ß2MG, and NAG. Among the 916 participants who had resided in the area before the soil restoration, urinary Cd concentrations were significantly higher, thus by 1.03-fold (95% CI, 1.01-1.04) in men and 1.03-fold (95% CI, 1.01-1.05) in women, when the years of residence before soil restoration by each 5-years increment. By contrast, urinary Cd concentrations were significantly lower, thus 0.97-fold (95% CI, 0.96-0.99) lower in men and 0.97-fold (95% CI, 0.95-0.99) lower in women, by each 5-year increment of residence after soil restoration. A similar association was observed for urinary ß2MG concentration, and no significant association was observed for urinary NAG levels in men or women. CONCLUSIONS: Cd exposure and associated renal tubular dysfunction in residents of a former Cd-polluted area were influenced by Cd exposure from the environment prior to soil restoration. Soil restoration in Cd-polluted areas reduced the Cd exposure of local residents.

Transcriptome analysis reveals the molecular mechanism of different forms of selenium in reducing cadmium uptake and accumulation in wheat seedlings.

Selenium (Se) can counteract cadmium (Cd) toxicity in wheat, but the molecular mechanism of different Se forms reducing Cd uptake and accumulation in wheat seedlings remain unclear. Here, a hydroponic experiment was conducted to investigate the effects of three Se forms (selenite (Se(IV)), selenate (Se(VI)) and seleno-L-methionine (SeMet)) on Cd2+ influx, Cd subcellular distribution, and Cd accumulation in wheat seedlings, and the underlying molecular mechanisms were investigated through transcriptome analysis. Consequently, Se(IV) and Se(VI) addition significantly reduced root Cd concentration by 74.3% and 80.8%, respectively, and all Se treatments significantly decreased shoot Cd concentration by approximately 34.2%-74.9%, with Se(IV) addition having the most pronounced reducing effect. Transcriptome analysis showed the reduction of Cd accumulation after Se(IV) addition was mainly due to the downregulation of Cd uptake genes. The inhibition of Cd accumulation after Se(VI) addition was not only associated with the downregulation of Cd uptake genes, but also related to the sequestration of Cd in vacuole. For SeMet addition, the reduction of Cd accumulation was mainly related to the sequestration of Cd in vacuole as GSH-Cd. The above findings provide novel insights to understand the effects of different forms of Se on Cd uptake and accumulation and tolerance in wheat.

The protective effects of chrysin on cadmium-induced pulmonary toxicity; a multi-biomarker approach.

This study aimed to determine the potential protective effects of chrysin (CHR) on experimental cadmium (Cd)-induced lung toxicity in rats. To this end, rats were divided into five groups; Control, CHR, Cd, Cd + CHR25, Cd + CHR50. In the study, rats were treated with CHR (oral gavage, 25 mg/kg and 50 mg/kg) 30 min after giving Cd (oral gavage, 25 mg/kg) for 7 consecutive days. The effects of Cd and CHR treatments on oxidative stress, inflammatory response, ER stress, apoptosis and tissue damage in rat lung tissues were determined by biochemical and histological methods. Our results revealed that CHR therapy for Cd-administered rats could significantly reduce MDA levels in lung tissue while significantly increasing the activity of antioxidant enzymes (SOD, CAT, GPx) and GSH levels. CHR agent exerted antiinflammatory effect by lowering elevated levels of NF-κB, IL-1ß IL-6, TNF-α, RAGE and NRLP3 in Cd-induced lung tissue. Moreover CHR down-regulated Cd-induced ER stress markers (PERK, IRE1, ATF6, CHOP, and GRP78) and apoptosis markers (Caspase-3, Bax) lung tissue. CHR up-regulated the Bcl-2 gene, an anti-apoptotic marker. Besides, CHR attenuated the side effects caused by Cd by modulating histopathological changes such as hemorrhage, inflammatory cell infiltration, thickening of the alveolar wall and collagen increase. Immunohistochemically, NF-κB and Caspase-3 expressions were intense in the Cd group, while these expressions were decreased in the Cd + CHR groups. These results suggest that CHR exhibits protective effects against Cd-induced lung toxicity in rats by ameliorating oxidative stress, inflammation, apoptosis, endoplasmic reticulum stress and histological changes.

Morin mitigates cadmium-induced testicular impairment by stimulating testosterone secretion and germ cell proliferation in mice.

Cadmium (Cd) is one of the heavy metal pollutants present in the environment due to human intervention. It is well known that Cd causes toxicological effects on various organs, including the testes. Morin hydrate is a plant-derived bioflavonoid with antioxidant, anti-inflammatory, and anti-stress properties. Thus, the question can be raised as to whether Morin has an effect on Cd-intoxication-induced testicular impairment. Therefore, the aim of this study was to investigate the role of Morin on Cd-mediated disruption of testicular activity. Mice were divided into three groups: group 1 served as the control group, group 2 was given Cd (10 mg/kg) orally for 35 days, and group 3 was given Cd and Morin hydrate (100 mg/kg) for 35 days. To validate the in vivo findings, an in vitro study on testicular explants was also performed. The results of the in vivo study showed that Cd-intoxicated mice had testicular disorganization, reduced circulating testosterone levels, decreased sperm density, and elevated oxidative stress and sperm abnormality. The expression of the germ cell proliferation marker, germ cell nuclear acidic protein (GCNA), and adipocytokine visfatin were also downregulated. It was observed that Morin hydrate upregulated testicular visfatin and GCNA expression in Cd-intoxicated mice, along with improvement in circulating testosterone, testicular histology, and sperm parameters. Furthermore, the in vitro study showed that Cd-mediated downregulation of testicular visfatin and GCNA expression, along with the suppressed secretion of testosterone from testicular explants, was normalized by Morin treatment, whereas visfatin expression was not. Overall, these data indicate that environmental cadmium exposure impairs testicular activity through downregulation of visfatin and GCNA expression, and Morin might play a protective role against Cd-induced testicular toxicity.

The Antioxidant Activity of Betanin protects MRC-5 cells Against Cadmium Induced Toxicity.

Cadmium (Cd) can induce both acute and chronic effects in the lungs depending on the time and the exposure route. Betanin is a component derived from the roots of red beets and it is well-known for its antioxidant and anti-apoptosis effects. The current study aimed to survey the protective effects of betanin on cell toxicity induced by Cd. Different concentration of Cd alone and in combination with betanin was assessed in MRC-5 cells. The viability and oxidative stress were measured using resazurin and DCF-DA methods respectively. Apoptotic cells were assessed by PI staining of the fragmented DNA and western blot analysis detected the activation of caspase 3 and PARP proteins. Cd exposure for 24 h declined viability and increased ROS production in MRC-5 cells compared to the control group (p < 0.001). Also, Cd (35 µM) elevated DNA fragmentation (p < 0.05), and the level of caspase 3-cleaved and cleaved PARP proteins in MRC-5 cells (p < 0.001). Co-treatment of cells with betanin for 24 h significantly enhanced viability in concentrations of 1.25 and 2.5 µM (p < 0.001) and 5 µM (p < 0.05) and declined ROS generation (1.25 and 5 µM p < 0.001, and 2.5 µM p < 0.01). As well as, betanin reduced DNA fragmentation (p < 0.01), and the markers of apoptosis (p < 0.001) compared to the Cd-treated group. In conclusion, betanin protects lung cells against Cd-induced toxicity through antioxidant activity and inhibition of apoptosis.

Asperuloside attenuates cadmium-induced toxicity by inhibiting oxidative stress, inflammation, fibrosis and apoptosis in rats.

This present study investigated the protective effects of asperuloside (ASP) against cadmium-induced nephrocardiac toxicity. Rats were treated with 50 mg/kg of ASP for five weeks and CdCl2 (5 mg/kg, p.o., once daily) during the last 4 weeks of ASP treatment. The serum levels of blood urea nitrogen (BUN), creatinine (Scr), aspartate transaminase (AST), creatine kinase-MB (CK-MB), troponin T (TnT) and lactate dehydrogenase (LDH) were evealuted. Oxido-inflammatory parameters were detected via malondialdehyde (MDA), reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), interleukin-1beta (IL-1ß) and nuclear factor kappa B (NF-κB). Additionally, the cardiorenal levels of caspase 3, transforming growth factor-ß (TGF-ß), α-smooth muscle actin (α-SMA), collagen IV and Bcl2 were measured by ELISA or immunohistochemical assays. The results indicated that ASP significantly decreased Cd-instigated oxidative stress, serum BUN, Scr, AST, CK-MB, TnT and LDH as well as histopathological alterations. Furthermore, ASP notably attenuated Cd-induced cardiorenal and apoptosis and fibrosis by reducing caspase 3 and TGF-ß levels, as well as reducing the stain intensity of a-SMA and collagen IV, while increasing Bcl2 intensity. These results revealed that ASP attenuated Cd induced cardiac and renal toxicity which may be attributed to reducing oxidative stress, inflammation, fibrosis and apoptosis.

Polymeric Interlayer in CdS-Free Electron-Selective Contact for Sb2Se3 Thin-Film Solar Cells.

High open-circuit voltage in Sb2Se3 thin-film solar cells is a key challenge in the development of earth-abundant photovoltaic devices. CdS selective layers have been used as the standard electron contact in this technology. Long-term scalability issues due to cadmium toxicity and environmental impact are of great concern. In this study, we propose a ZnO-based buffer layer with a polymer-film-modified top interface to replace CdS in Sb2Se3 photovoltaic devices. The branched polyethylenimine layer at the ZnO and transparent electrode interface enhanced the performance of Sb2Se3 solar cells. An important increase in open-circuit voltage from 243 mV to 344 mV and a maximum efficiency of 2.4% was achieved. This study attempts to establish a relation between the use of conjugated polyelectrolyte thin films in chalcogenide photovoltaics and the resulting device improvements.

Atorvastatin prevents cadmium-induced renal toxicity in a rat model.

In many industrial processes, worker exposure to cadmium causes kidney damage; thus, protection against cadmium toxicity is important in workplace health. Cadmium toxicity involves oxidative stress by increasing the levels of reactive oxygen species. Statins have shown antioxidant effects that might prevent this increase in oxidative stress. We investigated the potential effects of atorvastatin pretreatment in protecting experimental rats against kidney toxicity caused by cadmium. Experiments were performed on 56 adult male Wistar rats (200 ± 20 g), randomly assigned to eight groups. Atorvastatin was administered by oral gavage for 15 days at 20 mg/kg/day, starting 7 days before cadmium chloride intra-peritoneal administration (at 1, 2, and 3 mg/kg) for 8 days. On day 16, blood samples were collected, and kidneys were excised to evaluate the biochemical and histopathological changes. Cadmium chloride significantly increased malondialdehyde, serum creatinine, blood urea nitrogen, and decreased superoxide dismutase, glutathione, and glutathione peroxidase levels. Pre-administration of rats with atorvastatin at a dose of 20 mg/kg decreased blood urea nitrogen, creatinine, and lipid peroxidation, increased the activities of antioxidant enzymes, and prevented changes in physiological variables compared with animals that were not pretreated. Atorvastatin pretreatment prevented kidney damage following exposure to toxic doses of cadmium. In conclusion, atorvastatin pretreatment in rats with cadmium chloride-induced kidney toxicity could reduce oxidative stress by changing biochemical functions and thereby decreasing damage to kidney tissue.

Gallic acid abates cadmium chloride toxicity via alteration of neurotransmitters and modulation of inflammatory markers in Wistar rats.

Cadmium is a highly neurotoxic heavy metal that disrupts membranes and causes oxidative stress in the brain. The study aimed to investigate the neuroprotective effect of gallic acid on oxidative damage in the brains of Wistar rats exposed to cadmium chloride (CdCl2). Male Wistar rats were divided into four groups of five rats each. Group 1 was administered distilled water only throughout the study. Throughout the study, Group 2 received CdCl2 alone (5 mg/kg b.w./day), Group 3 received gallic acid (20 mg/kg b.w./day), and Group 4 received CdCl2 + gallic acid (20 mg/kg). Treatments were oral with distilled water as a vehicle. The study lasted 21 days. In the brain, the activities of cholinesterase and antioxidant enzymes were evaluated, as well as the levels of reduced glutathione, malondialdehyde, neurotransmitters, Na+/K+ ATPase, myeloperoxidase activity, nitric oxide, and interleukin-6. CdCl2-induced brain impairments in experimental animals and gallic acid prevents the following CdCl2-induced activities: inhibition of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE), elevated neurotransmitters (serotonin and dopamine), decreased antioxidant enzymes (superoxide dismutase, catalase), decreased glutathione, Na+/K+ ATPases, and increased MDA and neuroinflammatory markers (myeloperoxidase (MPO), nitric oxide, and interleukin-6 in the brain of experimental rats exposed to CdCl2 (p < 0.05). Taken together, the neuroprotective effects of gallic acid on CdCl2-induced toxicity in the brains of rats suggest its potent antioxidant and neurotherapeutic properties.

Different nanobubbles mitigate cadmium toxicity and accumulation of rice (Oryza sativa L.) seedlings in hydroponic cultures.

Cadmium (Cd) contamination can pose a severe threat to food production and human health. The accumulation of Cd in rice will decrease rice biomass, photosynthetic activity, and antioxidant capacity, affecting crop yield. The effects of different nanobubbles on the growth and Cd accumulation of rice seedlings under hydroponic conditions were investigated in this study. The results showed that the biomass, photosynthetic pigment content, and antioxidant enzyme activity of rice seedlings decreased when treated with Cd alone and that Cd induced lipid peroxidation in rice seedlings. However, when different types of nanobubbles were introduced into the nutrient solution, the bioavailability of Cd in the solution was reduced. As a result, the Cd content in rice was significantly decreased compared to treatment with Cd alone. Nanobubbles increased the biomass of rice, enhanced photosynthesis, and improved the antioxidant capacity of rice by increasing antioxidant enzyme activities to alleviate Cd-induced oxidative stress. At the same time, nanobubbles increased the Fe content in rice, which decreased the Cd content, as Cd is antagonistic to Fe. In conclusion, these results suggested that nanobubbles are a potential method of mitigating Cd stress that may help to improve rice yield and could be further explored in production.

Assessment soil cadmium and copper toxicity on barley growth and the influencing soil properties in subtropical agricultural soils.

Evaluation joint cadmium (Cd) and copper (Cu) phytotoxicity in wide range of subtropical agricultural soils is highly vital for phytoremediation of soils contaminated with Cd and Cu. In this study, barley root elongation assays were performed in 30 representative soils in response to single and combined Cd and Cu inhibition. The single Cd caused nearly 50% inhibition of barley root elongation, and Cu induced more than 50% inhibition in most soils. Mixed Cd + Cu caused significant inhibition on barley growth with average relative root elongation values of 20.0% and 30.4% in soil with a pH < 7 and pH > 7, respectively. An antagonistic interaction was evaluated in combined Cd + Cu toxicity, which was strong in soils containing low soluble Cu and Cd contents. Soil pH was the controlling factor in predicting single and mixed Cd and Cu phytotoxicity, which could explain 44% and 46% variation of single Cd and Cu toxicity, respectively. Soil organic carbon and effective cation exchange capacity were another important factor positively influencing metal toxicity, which further improved empirical prediction models accuracy, with determined coefficient (r2) values of 0.44-0.84. These results provide a theoretical basis for soils Cd and Cu pollution control.