Biometals最新文献

Cadmium (Cd) is an important environmental pollutant that poses a threat to human health and represents a critical component of air pollutants, food sources, and cigarette smoke. Cd is a known carcinogen and has toxic effects on the environment and various organs in humans. Heavy metals within an organism are difficult to biodegrade, and those that enter the respiratory tract are difficult to remove. Autophagy is a key mechanism for counteracting extracellular (microorganisms and foreign bodies) or intracellular (damaged organelles and proteins that cannot be degraded by the proteasome) stress and represents a self-protective mechanism for eukaryotes against heavy metal toxicity. Autophagy maintains cellular homeostasis by isolating and gathering information about foreign chemicals associated with other molecular events. However, autophagy may trigger cell death under certain pathological conditions, including cancer. Autophagy dysfunction is one of the main mechanisms underlying Cd-induced cytotoxicity. In this review, the toxic effects of Cd-induced autophagy on different human organ systems were evaluated, with a focus on hepatotoxicity, nephrotoxicity, respiratory toxicity, and neurotoxicity. This review also highlighted the classical molecular pathways of Cd-induced autophagy, including the ROS-dependent signaling pathways, endoplasmic reticulum (ER) stress pathway, Mammalian target of rapamycin (mTOR) pathway, Beclin-1 and Bcl-2 family, and recently identified molecules associated with Cd. Moreover, research directions for Cd toxicity regarding autophagic function were proposed. This review presents the latest theories to comprehensively reveal autophagy behavior in response to Cd toxicity and proposes novel potential autophagy-targeted prevention and treatment strategies for Cd toxicity and Cd-associated diseases in humans.

Inorganic arsenic is a well-known environmental toxicant, and exposure to this metalloid is strongly linked with severe and extensive toxic effects in various organs including the lungs. In the present study, we aimed to investigate the acute and chronic effects of arsenite exposure on pulmonary tissue in young and adult mice. In brief, young and adult female Balb/C mice were exposed to 3 and 30 ppm arsenite daily via drinking water for 30 and 90 days. Subsequently, the animals were sacrificed and various histological and immunohistochemistry (IHC) analyses were performed using lung tissues. Our findings showed arsenite was found to cause dose-dependent pathological changes such as thickening of the alveolar septum, inflammatory cell infiltrations and lung fibrosis in young and adult mice. In addition, arsenite exposure significantly increased the expression of inflammatory markers NF-κB and TNF-α, indicating that arsenite-exposed mice suffered from severe lung inflammation. Moreover, the IHC analysis of fibrotic proteins demonstrated an increased expression of TGF-β1, α-SMA, vimentin and collagen-I in the arsenite-exposed mice compared to the control mice. This was accompanied by apoptosis, which was indicated by the upregulated expression of caspase-3 in arsenite-exposed mice compared to the control. Adult mice were generally found to be more prone to arsenite toxicity during chronic exposure relative to their younger counterparts. Overall, our findings suggest that arsenite in drinking water may induce dose-dependent and age-dependent structural and functional impairment in the lungs through elevating inflammation and fibrotic proteins.

This study addresses the limited understanding of chromium-microbial mat interactions in estuarine tidal flats. The aims were to evaluate (1) the efficiency of the microbial consortium in Cr(III) removal from seawater; (2) the elemental and mineralogical composition of the microbial mat as a natural system in the Cr removal, (3) the effects of metal on microphytobenthos, and (4) possible interactions of Cr with other metals present in the consortium. Microbial mats were exposed to Cr(III) solutions at different concentrations (2–30 mg Cr/L). Analysis such as metal concentration, organic matter content, chlorophyll a and phaeopigment concentrations, abundance of diatoms and cyanobacteria, SEM-EDS, and XRD were performed. Most of the Cr(III) was deposited, as chromium oxide/hydroxide, on the surface of all microbial mat components. The complete microbial mat, comprising sediments, detritus, EPS, and diverse microorganism communities, exhibited a remarkable capacity to accumulate Cr(III), retaining over 87% in the solution.

The processed forms of milk, branded liquid, and power milk available in Dhaka city, the capital of Bangladesh, were investigated for essential and trace metal/metalloids regarding nutritional and human health risk aspects. For this, the potential nutritional contribution, estimated daily intake (EDI) and non-carcinogenic risk for six different life stages with male and female categories, as well as the carcinogenic risk for children and adults of both genders, were addressed. In total, 46 branded liquid and powder milk samples were considered for this analysis employing atomic absorption spectroscopy. The concentration of essential elements showed the trends of K > Ca > Na > Mg > Fe > Zn > Mn > Cu and K > Ca > Na > Mg > Fe > Cu > Mn > Zn for liquid and powder milk samples, respectively, but the potentially hazardous one showed the same trends (Cr > Pb > Hg > As > Cd) for both items. Except for Cr, Hg, and Fe, the elemental compositions of both milk categories differed considerably (< 0.05). Compared to the threshold values for milk samples (liquid and powder), Fe (19% and 27%), Mn (100% and 63%), Cu (0% and 23%), Zn (94% and 0%), Pb (25% and 13%), and Cr (0% and 3%) showed above the permissible limits. The nutrient input was the highest for Ca (27.2% and 18.7%), followed by Mg, K, and Na. The EDI of studied elements was within the daily permissible limit in both the milk category (except age group (≤ 3) and the female category). The non-carcinogenic risk assessment showed that the age groups ≤ 3 for liquid milk and ≤ 3 and 3 < X ≤ 14 with female categories for powder milk exceeded the threshold level (> 1) in the case of Cr, Cd, As, Zn, and Mn. The probable carcinogenic risks indicated an unacceptable risk level (< 1.00E-04) for the ingestion of Cr through powder milk samples for children in male and female categories. Finally, it believes that green cow farming practices and green milk processing technology, as well as continuous monitoring of toxic metals, can limit the ultimate risk worldwide.

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Aluminum is a potent neurotoxin, responsible for memory impairment and cognitive dysfunction. The neurotoxic effect of aluminum on cognitive impairment is well documented, however, exposure to aluminum in a time-dependent manner and post-exposure self-recovery still needs to be elaborated. This research aimed to (1) study the time-dependent effect of aluminum exposure by administering a total dose of 5850 mg/kg of Al over two different time periods: 30 and 45 days (130 and 195 mg/kg of AlCl₃ respectively), and (2) study 20 days post-exposure self-recovery effect in both aluminum-exposed groups by giving distilled water. Cognitive abilities were investigated through Morris water maze test and hole board test and compared in both exposure and recovery groups. Oxidative stress markers and neurotransmitter levels were measured for both exposure and recovery groups. To understand the mechanism of aluminum exposure and recovery, immunohistochemical analysis of synaptophysin (Syp) and glial fibrillary acidic protein (GFAP) was performed. Results showed cognitive dysfunction, oxidative stress-induced damage, reduced neurotransmitter levels, decreased immunoreactivity of Syp, and increased GFAP. However, these parameters showed a larger improvement in the recovery group where rats were given aluminum for 30 days period in comparison to recovery group followed by 45 days of aluminum exposure. These results suggest that restoration of cognitive ability is affected by the duration of aluminum exposure. The study findings provide us with insight into the adverse effects of aluminum exposure and can be utilized to guide future preventive and therapeutic strategies against aluminum neurotoxicity.

Cadmium (Cd⁺²) renders multifarious environmental stresses and highly toxic to nearly all living organisms including plants. Cd causes toxicity by unnecessary augmentation of ROS that targets essential molecules and fundamental processes in plants. In response, plants outfitted a repertory of mechanisms to offset Cd toxicity. The main elements of these are Cd chelation, sequestration into vacuoles, and adjustment of Cd uptake by transporters and escalation of antioxidative mechanism. Signal molecules like phytohormones and reactive oxygen species (ROS) activate the MAPK cascade, the activation of the antioxidant system andsynergistic crosstalk between different signal molecules in order to regulate plant responses to Cd toxicity. Transcription factors like WRKY, MYB, bHLH, bZIP, ERF, NAC etc., located downstream of MAPK, and are key factors in regulating Cd toxicity responses in plants. Apart from this, MAPK and Ca²⁺signaling also have a salient involvement in rectifying Cd stress in plants. This review highlighted the mechanism of Cd uptake, translocation, detoxification and the key role of defense system, MAPKs, Ca²⁺ signals and jasmonic acid in retaliating Cd toxicity via synchronous management of various other regulators and signaling components involved under stress condition.

The circulating micronutrient pattern in type 2 diabetes mellitus (T2DM) may impact glycemic control and insulin resistance; however, there is a scarcity of studies that have evaluated the circulating micronutrient pattern in the T2DM population. Therefore, our objective was to identify circulating micronutrient pattern and their association with markers of glycemic control and insulin resistance in individuals with T2DM. We developed a cross-sectional observational study involving adults with T2DM in Sergipe, Brazil. We assessed plasma levels of magnesium, zinc, calcium, potassium, and serum 25-hydroxyvitamin D. Additionally, also measured fasting glucose levels, the percentage of glycated hemoglobin (%HbA1c), and calculated the homeostatic model assessment for insulin resistance (HOMA-IR). Patterns of body reserve were established using principal component analysis and categorized into quartiles. Binary logistic regression models were employed. We evaluated 114 individuals (63.7% women), with a median age and body mass index of 49 years and 29.6 kg/m², respectively. Two circulating micronutrient patterns were identified, explaining 62.5% of the variance: Pattern 1 (positive contributions from magnesium, zinc, calcium, and potassium) and Pattern 2 (positive contributions from 25-hydroxyvitamin D and zinc, with a negative contribution from potassium). Lowest quartile for Pattern 1 and Pattern 2 exhibiting a 4.32-fold (p = 0.019) and 3.97-fold (p = 0.038) higher likelihood of increasing HOMA-IR and %HbA1c values, respectively, compared to the larger quartiles. However, no associations were found between these patterns and fasting glucose values. Lowest quartile for both patterns of micronutrients was associated with inadequate metabolic control in individuals with T2DM.

There is limited experimental evidence on the biochemical consequences of aluminium (Al) and cadmium (Cd) co-exposures during pregnancy and postnatal life.This study investigated the impacts of perinatal Al chloride (AlCl₃) and Cd chloride (CdCl₂) co-exposures on neuroendocrine functions in mice offspring during postnatal life. The study comprised of four pregnant experimental groups. Group 1 received AlCl₃ (10 mg/kg), group 2 were administered CdCl₂ (1.5 mg/kg), while group 3 received both AlCl₃ (10 mg/kg) and CdCl₂ (1.5 mg/kg) (AlCl₃+CdCl₂), and group 4 received saline (10 mL/kg) only and served as control group. All experimental animals were chemically exposed once daily from gestation days 7–20. Upon delivery, male pups were regrouped based on maternal chemical exposure on postnatal day 21 (PND 21) and allowed to grow to adulthood until PND 78, after which they were sacrificed for assessment of neuroendocrine markers and histological investigations. There was no statistical significance (p > 0.05) on follicle stimulating hormone, testosterone, estrogen and progesterone, thyroid stimulating hormone, thyroxine (T4) in all treatment groups relative to controls|. However, AlCl₃ and AlCl₃-CdCl₂ significantly (p < 0.05) reduced triiodothyronine (T3) levels, with a profound increase in T3:T4 ratio by AlCl₃, and AlCl₃+CdCl₂ compared to control. Furthermore, pups from pregnant mice treated with CdCl₂ and AlCl₃+CdCl₂ demonstrated increased testicular malondialdehyde concentration with increased catalase activity relative to controls, suggesting oxidative imbalance. In addition, AlCl₃, CdCl₂, and AlCl₃+CdCl₂ exposures induced testicular and hypothalamic architectural disruption compared to controls, with marked architectural derangement in the AlCl₃+CdCl₂ group. Our findings suggest that prenatal co-exposures to Alcl₃ and CdCl₂ induce testicular and hypothalamic alterations in offspring via a testicular oxidative stress and thyrotoxicosis-dependent mechanisms.

Dietary cadmium (Cd²⁺) intake is implicated in the pathogenesis of hypertension and anaemia, but there is a paucity of information on the haematological changes in hypertensive conditions. This study, therefore, aims to evaluate the effects of Cd²⁺ on blood pressure (BP) and haematological indices in the Sprague–Dawley rat model. Three cohorts (n = 10 each) of control and Cd²⁺-fed male Sprague–Dawley rats were selected. Cd²⁺-exposed rats received 2.5 or 5 mg/kg b.w. cadmium chloride via gavage thrice-weekly for eight weeks, while control animals received tap water. BP and flow were measured non-invasively from rat tails twice-weekly using a CODA machine, while weights were measured thrice-weekly. Haematological indices were assessed using the Cell-Dyn Emerald Haematology Analyzer. Data were reported as mean ± SEM, and statistically analyzed using One-Way Analysis of Variance. Bonferroni post hoc test was used for multiple comparisons. Cd²⁺-exposure induced hypertension by significantly (p < 0.05) elevating systolic, diastolic, and mean arterial BPs, pulse pressure, and heart rate (HR), and increased (p < 0.05) blood flow. Mean cell volume (MCV) and haemoglobin (MCH) were significantly (p < 0.05) reduced, and red cell distribution width (RDW) significantly (p < 0.01) increased by exposure to 5 mg/kg b.w. Cd²⁺. Haemoglobin concentration (MCHC), haematocrit, haemoglobin, red blood cell, platelet, mean platelet volume, and white blood cell counts were unaffected by Cd²⁺-exposure. Cd²⁺ induced hypertension, microcytosis, hypochromicity, and anisocytosis without anaemia, which may be precursor to microcytic anaemia and coronary artery disease. This study is important in Cd²⁺-exposed environments and warrants further investigations.