Cadmium Exposure Research Articles

Salicylic acid priming before cadmium exposure increases wheat growth but does not uniformly reverse cadmium effects on membrane glycerolipids.

Cadmium (Cd) is an abiotic stressor negatively affecting plant growth and reducing crop productivity. The effects of Cd (25 μM) and of pre-soaking seeds with salicylic acid (SA) (500 μM) on morphological, physiological, and glycerolipid changes in two cultivars of wheat (Triticum aestivum L. 'Tosunbey' and 'Cumhuriyet') were explored. Parameters measured were length, fresh and dry biomass, Cd concentration, osmotic potential (ψ), lipid peroxidation, and polar lipid species in roots and leaves, as well as leaf chlorophyll a, carotenoids, and fv/fm. Fresh biomass of roots and leaves and leaf length were strongly depressed by Cd treatment compared to the control, but significantly increased with SA + Cd compared to Cd alone. Cd reduced leaf levels of chlorophyll a, carotenoids, and fv/fm, compared to controls. Treatment with SA + Cd increased pigment levels and fv/fm compared to Cd alone. Cd treatment led to a decrease in DW of total membrane lipids in leaves and depressed levels of monogalactosyldiacylglycerol and phosphatidic acid in leaves and roots of both cultivars. The effects of SA priming and SA + Cd treatment on lipid content and composition were cultivar-specific, suggesting that lipid metabolism may not be a primary target underlying SA remediation of the damaging effects of Cd on wheat growth and development.

Assessing the effects of cadmium on antioxidant enzymes and histological structures in rainbow trout liver and kidney

Cadmium contamination in aquatic environments poses severe risks to aquatic organisms, particularly fish, where cadmium accumulation in tissues can lead to compromised organ functionality and reproductive issues. The present study aimed to assess the effects of cadmium (Cd) exposure on key biomarkers of oxidative stress, DNA damage, apoptosis, and enzyme activity in the liver and kidney tissues of rainbow trout (Oncorhynchus mykiss). Specifically, the study measured 8-hydroxy-2-deoxyguanosine (8-OHdG) levels, caspase-3 activation, acetylcholinesterase (AChE) activity, and oxidative stress indicators (ONOO−, MDA, GSH, SOD, and CAT) following exposure to three Cd concentrations (1, 3, and 5 mg/L) over three time points (24, 48, and 96 h). Tissue samples were collected post-exposure, and the analysis revealed a significant decrease in MDA levels in both tissues. GSH concentrations declined with prolonged exposure, while SOD activity increased, indicating a response to oxidative stress, contrasted by a reduction in CAT activity. An initial increase in ONOO− levels was observed at 24 h, followed by a subsequent decrease at the 48 and 96 h marks. These results suggest that cadmium induces oxidative stress in the liver and kidney tissues of fish. Cadmium exposure also significantly elevated 8-OHdG levels, signaling DNA damage, and increased caspase-3 activity, indicative of apoptosis, across all doses and time points (p < 0.05). The histological examination of liver and kidney showed tissue injury. Additionally, a negative correlation between AChE activity and exposure duration was noted, with prolonged exposure resulting in substantial AChE inhibition. Given the role of AChE in behavior regulation, these findings underscore the importance of exploring time-dependent, tissue-specific changes in AChE activity to further elucidate the mechanisms underlying cadmium-induced behavioral abnormalities.

S-nitrosoglutathione reductase disfavors cadmium tolerance in shoots of Arabidopsis

S-nitrosoglutathione reductase (GSNOR) is involved in the response to cadmium (Cd) exposure. In this study, the plants of mutant (gsnor1-3) with lossing-function of- and over-expression (GSNOROE5) of GSNOR were used to clear the role of GSNOR in Cd tolerance. GSNOR activity increased through upregulating the expression of the AtGSNOR gene and protein in Arabidopsis thaliana under Cd stress, which attenuated Cd tolerance. Oxidative damage was more serious in GSNOROE5 and was alleviated in gsnor1-3 under Cd stress, compared with Col-0. Induction of GSNOR facilitated H2O2 accumulation but inhibited catalase (CAT) activity in shoots under Cd stress. This phenotype was eliminated by 3-amino-1,2,4-triazole (3-AT), a CAT inhibitor. In addition, the expressions of AtCAT1 and AtCAT2 were down-regulated with increasing GSNOR activity under Cd stress. This suggested that GSNOR was involved in the accumulation of hydrogen peroxide (H2O2) through regulating CAT expression and activity under Cd exposure. Furthermore, Cd tolerance and CAT activity were improved by spraying S-nitrosoglutathione (GSNO) onto the surface of the leaves. The in vitro activity of CAT increased with GSNO concentration until a GSNO/CAT ratio of 2 was reached. Thus, CAT activity was relative to GSNOR through regulating the expression and S-nitrosylation level of proteins. In summary, the Cd-induced promotion of GSNOR activity aggravated Cd toxicity in plants by mediating H2O2 accumulation controlled by CAT.

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.

Cadmium exposure and hypertension: a systematic review and a dose-response meta-analysis

Abstract Background Since the shape of the relation between Cd exposure and risk of HTN has not been previously investigated, we aimed to perform a systematic review with dose-response meta-analysis in epidemiological studies. Methods After registration of the review in PROSPERO database (ID: CRD42022382030), we searched for eligible articles in online databases using Mesh-terms/keywords related to Cd, HTN, and BP. Eligible criteria were: adult population, assessment of exposure through Cd concentrations in blood or urine, risk estimates for HTN, observational design. Whenever possible, we computed summary odds ratio (OR) with 95% confidence interval (CI) and performed a dose-response meta-analysis on overall studies and subgroups. Results We eventually included 8 articles for both the qualitative and quantitative analysis published between 2006-2023 almost of cross-sectional design, 7 and 4 assessing blood and urine Cd concentrations, respectively. Comparing the highest versus lowest exposure, we found increased risk of HTN for both blood (OR = 1.12, 95% CI 0.92-1.36) and urine assessment (OR = 1.09, 95% CI 0.94-1.28). Dose-response meta-analysis showed an almost linear increased risk for blood Cd concentrations until 1.5 µg/L above with it plateaued. In contrast when using urine concentrations for exposure assessment, risk started to increase above 0.5 µg/g creatinine. Conclusions Our results confirm the recent findings of non-linear relation between Cd exposure and risk of both CVD and diabetes and the subsequent need to lower Cd exposure on a public health perspective. Key messages • Cadmium exposure showed positive association with risk of hypertension. • Public health efforts should be implemented to lowed cadmium exposure to decrease CVD risk.

Geospatial clustering of auto-antibodies against apolipoprotein A-1, heavy metals, cardiovascular and liver diseases in the general population

Abstract Aims Heavy metals (HM) are combustion-related environmental factors predisposing to cardiovascular (CVD), autoimmune and liver diseases, even below regulatory concentrations. Pro-atherogenic and pro-steatotic auto-antibodies against apolipoprotein A1 (AAA1) are prevalent in the general population for unclear reasons. We explored a putative interplay between HM exposure, AAA1, CVD risk factors and a non-alcoholic fatty liver disease (NAFLD) risk score, using a geospatial clustering approach at the general population level. Methods Getis-Ord, Moran I2 clustering and geographically weighted regression (GWR) geosptatial analyses were carried out on 6361 individuals recruited in the CoLaus/PsyCoLaus general population cohort. Geospatial dependences between serum AAA1, urinary HM (cadmium, arsenic, cobalt) concentrations, SCORE2 CVD risk, and fatty liver index (FLI) were assessed. Results Cadmium and cobalt were found to be associated with higher SCORE2 risk (p&amp;lt;0.04). AAA1 were associated with higher cadmium, cobalt, and cigarette consumption, independently of SCORE2 (p&amp;lt;0.04). AAA1 hotspots overlapped significantly with those of cadmium and FLI, independently of SCORE2. According to GWR, correlations between cadmium and AAA1 were the highest in railways proximity regions, increasing up to 10-fold compared to global associations. AAA1 were not associated with other HM. Conclusions These geospatial footprints highlight independent associations between Cadmium, AAA1, and NAFLD risk score in the general population. We hypothesize that environmental cadmium exposure may facilitate the occurrence of AAA1 in humans. Ongoing experimental studies will confirm/refute a possible causal link. Whether AAA1 could represent an early biological signature of cadmium exposure and subsequent health hazards remains to be shown.

Blood cadmium levels and overactive bladder in middle-aged and older adults in the United States: Insights from NHANES 2007–2020 data

Cadmium is a common environmental pollutant associated with various health risks. Its neurotoxic, muscle-damaging, and pro-inflammatory properties may be related to overactive bladder (OAB), though few studies have assessed its impact on urinary function. This study aimed to examine the potential link between cadmium exposure and OAB. Using data from the 2007–2020 National Health and Nutrition Examination Survey (NHANES), we analyzed adults aged 40 and older (n = 15,467) in a cross-sectional design. OAB was defined by the refined Overactive Bladder Symptom Score (OABSS). Weighted multivariate logistic regression examined the associations between blood cadmium levels and OAB and its components. Age and gender stratifications were performed, and restricted cubic splines (RCS) were used to explore non-linear associations between blood cadmium and OAB. Sensitivity analyses and co-exposure analyses with other pollutants were conducted to assess OAB definition stability, subgroup differences, and exposure collinearity. The prevalence of OAB was 26.2%. While blood cadmium showed a small, non-significant positive association with overall OAB, it was inversely associated with nocturia severity (OR = 0.85, 95% CI 0.74–0.98, p < 0.05). Blood cadmium was also linked to more severe urinary incontinence in the 50–59 age group and among non-Hispanic Black adults. A non-linear association between blood cadmium and OAB was observed (p for nonlinearity = 0.016, p < 0.05). In co-exposure analyses, cadmium remained a dominant and independent factor. These findings suggest that cadmium exposure may have a complex association with OAB and may relate differently to its various components. Further research is needed to explore these relationships.

Neurobehavioral and bioaccumulative toxicity in adult in-vivo zebrafish model due to prolonged cadmium exposure in the presence of ketoprofen.

Increasing industrial activity causes the release of chemical compounds into aquatic habitats, including toxic heavy metals like cadmium and medications like ketoprofen, posing considerable ecological concerns. Although previous studies have shown that cadmium and ketoprofen individually cause cognitive impairment, there is a lack of information on the combined neurological effects of the two substances. We investigated the neurological consequences of persistent cadmium exposure in the presence of ketoprofen on adult zebrafish, providing an essential model for understanding cumulative impacts on vertebrate organisms. Behavioral assessments, bioaccumulation rates, biochemical studies, and histopathological exams were conducted over 42 days in authentic environmental settings. The results of our study show that cadmium (10 µg/L) and ketoprofen (10 and 100 µg/L) at environmentally relevant concentrations had a significant impact on locomotor activity, social interactions, and cognitive responses, indicating cumulative neurotoxicity in co-exposure groups compared to single pollutant groups. Biochemical tests show disturbances in antioxidant defense systems, while histological examinations reveal structural changes in zebrafish brain regions. Ketoprofen influences cadmium accumulation in the brain, underscoring the importance of conducting complete evaluations to understand the intricate interactions between environmental pollutants. This study improves our understanding of the complex interactions between heavy metals and medications, stressing the need to consider combined exposure when assessing the neurological effects on vertebrate models.

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.

Cytoprotection against Cadmium by Nrf2-Activating Dietary Phytochemicals

In context with previous work by others, the present findings indicate that rosemary-based dietary supplement products like PB123 might promote beneficial responses against environmental cadmium exposure.

Epigenetic Modifications Are Involved in Transgenerational Inheritance of Cadmium Reproductive Toxicity in Mouse Oocytes

Maternal cadmium exposure during pregnancy has been demonstrated to have detrimental effects on offspring development. However, the impact of maternal cadmium exposure on offspring oocytes remains largely unknown, and the underlying mechanisms are not fully understood. In this study, we found that maternal cadmium exposure during pregnancy resulted in selective alteration in epigenetic modifications of mouse oocytes in offspring, including a decrease in H3K4me2 and H4K12ac, as well as an increase in DNA methylation of H19. Although ROS levels and mitochondrial activity remain at normal levels, the DNA damage marker γH2AX was significantly increased and the DNA repair marker DNA-PKcs was remarkably decreased in offspring oocytes from maternal cadmium exposure. These alterations are responsible for the decrease in the quality of mouse oocytes in offspring induced by maternal cadmium exposure. As a result, the meiotic maturation of oocytes and subsequent early embryonic development are influenced by maternal cadmium exposure. RNA-seq results showed that maternal cadmium exposure elicits modifications in the expression of genes associated with metabolism, signal transduction, and endocrine regulation in offspring ovaries, which also contribute to the disorders of oocyte maturation and failures in early embryonic development. Our research provides direct evidence of transgenerational epigenetic inheritance of cadmium reproductive toxicity in mouse germ cells.

Physical activity modified the association of blood cadmium and lead with Helicobacter pylori infection: A cross-sectional analysis with NHANES data.

Cadmium (Cd) and lead (Pb) exposure have been identified as risk factors for Helicobacter pylori seropositivity, possibly due to the immune suppression by Cd and Pb. Physical activity (PA) can induce an immune response. However, whether PA can reduce the effect of Cd and Pb on H pylori infection remains elusive. This study aims to investigate the association of blood Cd and Pb levels with H pylori infection and explore the intermediary effects of PA. This cross-sectional survey was conducted using the National Health and Nutrition Examination Survey (NHANES) of the 1999 to 2000 cycle (n = 9965). Participants without clear serological testing data, or absent in PA, blood Cd, and Pb information were excluded. Collinearity analysis was performed to remove the variables with high collinearity. Restricted cubic spline curve analysis was adopted to assess the nonlinear association of Cd and Pb with H pylori infection. The logistic regression analysis, generalized linear models, sensitivity analysis, and P for trend test were used to further analyze their relationship. Then, we analyzed the association of Cd and Pb with H pylori infection in 2 PA groups. Totally 3638 participants were divided into H pylori-negative (n = 2545) and H pylori-positive group (n = 1093). Pb exhibited a linear relationship but Cd had a nonlinear relationship with H pylori infection. Besides, the elevation of Cd and Pb both independently predicted H pylori infection after adjusting various variables (P < .05). The robust relationship was confirmed by the P for trend test (P for trend < .05). Under Cd exposure, the risk of H pylori infection was lower in the active PA group than in the inactive group (P < .05). A reverse result was found under the Pb exposure (P < .05). Exposure to Cd and Pb are positively linked to H pylori infection. PA may alleviate the effect of Cd on H pylori infection but may enhance H pylori infection under Pb exposure. Therefore, PA should be recommended in the appropriate season or region.

Health risk assessment of lead and cadmium exposure from food and snuff in Pakistani population

BackgroundSmokeless tobacco (SLT) is a tobacco-based product consumed without burning or smoking. Snuff, commonly known as naswar, is a widely used SLT product in Pakistan. This study is designed to investigate the concentrations of lead (Pb) and cadmium (Cd) in snuff and their associated health risks to consumers. MethodsBlood samples from snuff consumers and non-consumers were analyzed for Pb and Cd concentrations. Additionally, samples of drinking water and wheat flour were also analyzed for Pb and Cd. Health risk assessments were calculated using hazard quotient (HQ) and incremental lifetime cancer risk (ILCR) for Pb and Cd. ResultsSnuff consumers had significantly higher blood-Pb and blood-Cd levels compared to non-consumers. Approximately 38.5 % of snuff consumers were found to exceed blood-Pb levels from the safe limits (10 µg dL⁻¹) of the World Health Organization (WHO), while 48.9 % of snuff consumers were found to exceed blood-Cd levels from the WHO safe range of 0.03–0.12 µg dL⁻¹. Snuff samples contained Pb and Cd concentrations ranging from 5.3 to 22.4 µg g⁻¹ and 0.5–2.2 µg g⁻¹, respectively. Drinking water and wheat flour samples were found within the safe limits for Pb and Cd concentration, suggesting snuff as the primary source of exposure. Health risk assessments indicated elevated HQ values, for Pb (38.9 %) and Cd (14.3 %) detected in snuff, surpassing the safe HQ threshold of 1. Concerning ILCR from snuff, values for Pb were within the acceptable range, but alarmingly 100 % of samples for Cd exceeded the safe limits of USEPA (1.0×10⁻⁴), indicating a significant cancer risk in snuff users. ConclusionThis study highlights the exceeded Pb and Cd concentrations in snuff as well as also reporting significant carcinogenic and non-carcinogenic health risks to consumers. These findings emphasized the urgent need for regulatory bodies to ensure the safety of snuff before selling in the market. Public Health Professionals should also initiate educational campaigns to raise awareness among consumers and manufacturers about various health risks associated with the snuff.

High cadmium exposure impairs adult hippocampal neurogenesis via disruption of store-operated calcium entry

Cadmium (Cd) is a neurotoxicant that gradually accumulates in the human body with age. High Cd burden is correlated with adult hippocampal neurogenesis (AHN) and memory deficits in mammals. However, little knowledge is known about the mechanism by which Cd exposure impairs neurogenesis and cognition. Here, we investigated the roles of store-operated calcium entry (SOCE)-mediated calcium dyshomeostasis in Cd-induced AHN and memory deficits as well as therapeutic potential for the prevention of Cd-induced neurotoxicity. To achieve this goal, 8 weeks-old C57BL/6 J mice were subjected to different concentrations of cadmium chloride (0, 5, 10, 20 ppm) in drinking water for 8 weeks, we then examined the AHN, calcium homeostasis, SOCE channel and memory in Cd-exposed mice by using immunohistochemistry, calcium imaging, Y-maze and fear conditioning test. Our results indicated that chronic Cd exposure markedly increased Cd levels in serum and cerebrospinal fluid by almost 10-fold, and inhibited the proliferation and differentiation of hippocampal adult neural stem cells in a dose-dependent manner. Additionally, Cd exposure impaired the maturation of hippocampal neural stem cells without inducing gliosis. Transcriptome analysis revealed that Cd exposure inhibited the proliferation of neuroblastoma via alteration of calcium signaling pathway, and attenuated SOCE channels played a pivotal role in mediating Cd-induced cytoplasmic calcium overload and depletion of endoplasmic reticulum calcium stores. Activation of SOCE by hyperforin, a natural derivative from medicinal plant, restored intracellular calcium homeostasis and improved AHN and memory in Cd-exposed mice. Together, this study provided novel insights into the mechanism that Cd exposure impaired AHN and memory by prompting neuronal SOCE-mediated calcium dyshomeostasis, and offered a new therapeutic approach for prevention of Cd-induced neurotoxicity.

Potential pathogenic roles of ferroptosis and cuproptosis in cadmium-induced or exacerbated cardiovascular complications in individuals with diabetes.

Diabetes and its complications are major diseases that affect human health. Diabetic cardiovascular complications such as cardiovascular diseases (CVDs) are the major complications of diabetes, which are associated with the loss of cardiovascular cells. Pathogenically the role of ferroptosis, an iron-dependent cell death, and cuproptosis, a copper-dependent cell death has recently been receiving attention for the pathogenesis of diabetes and its cardiovascular complications. How exposure to environmental metals affects these two metal-dependent cell deaths in cardiovascular pathogenesis under diabetic and nondiabetic conditions remains largely unknown. As an omnipresent environmental metal, cadmium exposure can cause oxidative stress in the diabetic cardiomyocytes, leading to iron accumulation, glutathione depletion, lipid peroxidation, and finally exacerbate ferroptosis and disrupt the cardiac. Moreover, cadmium-induced hyperglycemia can enhance the circulation of advanced glycation end products (AGEs). Excessive AGEs in diabetes promote the upregulation of copper importer solute carrier family 31 member 1 through activating transcription factor 3/transcription factor PU.1, thereby increasing intracellular Cu+ accumulation in cardiomyocytes and disturbing Cu+ homeostasis, leading to a decline of Fe-S cluster protein and reactive oxygen species accumulation in cardiomyocytes mitochondria. In this review, we summarize the available evidence and the most recent advances exploring the underlying mechanisms of ferroptosis and cuproptosis in CVDs and diabetic cardiovascular complications, to provide critical perspectives on the potential pathogenic roles of ferroptosis and cuproptosis in cadmium-induced or exacerbated cardiovascular complications in diabetic individuals.

Cadmium-induced lung injury disrupts immune cell homeostasis in the secondary lymphoid organs in mice

Cadmium is a well-known toxic heavy metal that poses significant health risks, particularly through inhalation, smoking, and the consumption of contaminated food. Exposure to cadmium is linked to the development and exacerbation of chronic lung diseases such as pulmonary fibrosis and chronic obstructive pulmonary disease (COPD). This study investigated the systemic effects of intratracheal cadmium chloride (0.5mg/kg) instillation in C57BL/6 mice. All parameters, including inflammation assessment, lung function evaluation (using Flexi-vent), and immunophenotyping of T-cells in secondary lymphoid organs (spleen and mediastinal lymph nodes), were analyzed 14 days after Cd exposure. The results demonstrated that cadmium exposure led to significant immune cell infiltration in bronchoalveolar lavage (BAL) fluid, altered pro-inflammatory cytokine levels, and was associated with impaired lung function, characterized by increased lung resistance and Newtonian resistance. Analysis of T-cell populations revealed no significant changes in total T-cells in mediastinal lymph nodes and spleen, but a decrease in CD4+ T-cells and an increase in CD8+ T-cells were observed. These findings suggest that cadmium disrupts T-cell homeostasis in secondary lymphoid organs. Further research is crucial to elucidate the mechanisms underlying cadmium-induced lung injury and immune dysregulation, essential for developing effective therapeutic interventions against chronic lung diseases caused by cadmium exposure.

Chronic mild cadmium exposure increases the vulnerability of tomato plants to dehydration

Heavy metal contamination increases plant susceptibility to both biotic and abiotic stresses. However, the comprehensive impact of heavy metal pollution on plant hydraulics, which is crucial for plant productivity, and the interaction between heavy metal stress and environmental factors on plant health are not yet fully understood. In this study, we investigated the effects of cadmium exposure on plant-water relations and hydraulics of Solanum lycopersicum L., cultivar Piccadilly. Particular attention was given to leaf hydraulic conductance (KL) in response to cadmium pollution and dehydration.Cadmium exposure exhibited negligible impacts on tomato productivity but resulted in significant differences in pressure-volume derived traits. Leaves and roots of Cd-treated plants showed reduced wall stiffness compared to control samples. However, Cd-treated leaves had a less negative turgor loss point (Ψtlp), whereas Cd-treated roots exhibited more negative Ψtlp values due to lower osmotic potential at full turgor compared to control samples.Leaves and root cells of Cd-treated plants showed higher values of saturated water content compared to control plants, along with a distinct mineral profile between the two experimental groups. Despite similar leaf water potential thresholds for 50% and 80% loss of KL in control and cadmium-treated leaves, plants grown in cadmium-polluted soil showed higher leaf cell damages even under well watered conditions. This, in turn, affected the plant ability to recover from drought upon rehydration by compromising cell rehydration ability.Overall, the present findings suggest that under conditions of low water availability, cadmium pollution increases the risk of leaf hydraulic failure.

Risk Assessment of Cadmium (Cd) and Chromium (Cr) Exposure from Bosowa Cement Industry Emissions to Water Sources Utilized in Maros

Risk Assessment of Cadmium (Cd) and Chromium (Cr) Exposure from Bosowa Cement Industry Emissions to Water Sources Utilized in Maros

Liquid chromatography–mass spectrometry profiling of propolis and royal jelly and their ameliorative effects on cadmium-instigated pathological consequences in ovarian tissues of rats

This study was undertaken to identify the bioactive components of propolis (PRO) and royal jelly (ROJ) and their therapeutic influence on attenuating cadmium chloride (CdCl2)-induced ovarian toxicity and dysfunction in rats. The composition of PRO or ROJ was ascertained employing the liquid chromatography–linear ion trap quadrupole–mass spectrometry (LC–LTQ–MS–MS) method. To further evaluate the anti-infertility properties of PRO and ROJ instigated by cadmium (Cd) in vivo, thirty female mature rats (183.3 ± 12.5 g) were randomly assigned into six groups (n = 5 per group). The established animal groups included (I) control, (II) Cd, (III) PRO, (IV) ROJ, (VI) PRO + Cd, and (VII) ROJ + Cd groups. Cadmium exposure disrupted ovarian tissue functions, demonstrating remarkable disorders in progesterone and estrogen. Furthermore, the comet assay exhibited a marked rise in DNA impairment in Cd-exposed rats, implying genotoxicity. Conversely, PRO or ROJ significantly counteracted the Cd-instigated pathophysiological consequences, ameliorating hormonal levels and lessening DNA damage. Critically, histological analysis revealed several anomalies in the ovarian tissues of the Cd-administered group. Interestingly, PRO or ROJ preserved the typical structure of ovarian tissues. Our findings indicate that both PRO and ROJ could be utilized to attenuate the pernicious influences incited by Cd due to their anti-androgenic attributes.

Cadmium-induced fetal erythropoiesis disturbances in mice

Maternal anemia has been identified as a contributing factor to adverse reproductive outcomes associated with cadmium (Cd) exposure, a common heavy metal. Our recent findings suggest that inhibited erythroid differentiation and enucleation also play significant roles in the direct embryonic toxicity resulting from maternal Cd exposure. However, the effects of Cd exposure on lipid metabolism remodeling, which is essential for physiological erythropoiesis, remain poorly understood. In the present study, pregnant mice were administered low doses of CdCl2 via oral exposure from early to late gestation to mitigate Cd-induced maternal anemia. Compared to vehicle-treated controls, embryos from Cd-treated mice exhibited a slight decrease in weight, though without signs of atrophy. Consistent with our previous observations, fetal livers from Cd-exposed embryos demonstrated a dose-dependent inhibition of erythroid differentiation, as confirmed by ex vivo analysis. Notably, an intrinsic decrease in lipid peroxidation during erythroid differentiation was observed in the bone marrow and fetal livers of vehicle-treated mice, attributed to diminished lipid content. In contrast, this decrease in lipid peroxidation was absent in fetal liver erythroblasts from Cd-treated mice, where an increase in lipid peroxidation was instead noted. These findings elucidate a potential mechanism, lipid peroxidation, underlying Cd-induced embryonic toxicity.