Subacute cadmium exposure changes different metabolic functions, leading to type 1 and 2 diabetes mellitus features in female rats.

Cadmium (Cd) is a heavy metal that acts as endocrine disrupting chemical (EDC). Few studies have investigated the effects of Cd exposure on metabolic dysfunctions, such as type 1 and 2 diabetes mellitus (T1DM and T2DM). Thus, we assessed whether subacute Cd exposure at occupational levels causes abnormalities in white adipose tissue (WAT), liver, pancreas, and skeletal muscle. We administered cadmium chloride (CdCl2) (100 ppm in drinking water for 30 days) to female rats and evaluated Cd levels in serum and metabolic organs, morphophysiology, inflammation, oxidative stress, fibrosis, and gene expression. High Cd levels were found in serum, WAT, liver, pancreas, and skeletal muscle. Cd-exposed rats showed low adiposity, dyslipidemia, insulin resistance, systemic inflammation, and oxidative stress compared to controls. Cd exposure reduced adipocyte size, hyperleptinemia, increased cholesterol levels, inflammation, apoptosis and fibrosis in WAT. Cd-exposed rats had increased liver cholesterol levels, insulin receptor beta (IRß) and peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC1α) expression, karyomegaly, inflammation, and fibrosis. Cd exposure reduced insulin levels and pancreatic islet size and increased inflammation and fibrosis. Cd exposure reduced skeletal muscle fiber diameter and increased IR expression and inflammation. Finally, strong positive correlations were observed between serum, tissue Cd levels, abnormal morphology, tissue inflammation and fibrosis. Thus, these data suggest that subacute Cd exposure impairs WAT, liver, pancreas and skeletal muscle function, leading to T1DM and T2DM features and other complications in female rats.

A one-class classification approach for authentication of specialty coffees by inductively coupled plasma mass spectroscopy (ICP-MS).

Due to the lucrative nature of specialty coffees, there have been instances of adulteration where low-cost materials are mixed in to increase the overall volume, resulting in illegal profit. A widely used and recommended approach to detect possible adulteration is the application of one-class classifiers (OCC), which only require information about the target class to build the models. Thus, this work aimed to identify adulterations in specialty coffees with low-quality coffee using multielement analysis determined by ICP-MS and to evaluate the performance of one-class classifiers (dd-SIMCA, OCRF, and OCPLS). Therefore, authentic specialty coffee samples were adulterated with low-quality coffee in 25 % to 75 % (w/w) proportions. Samples were subjected to acid decomposition for analysis by ICP-MS. OCPLS method presented the best performance to detect adulterations with low-quality coffee in specialty coffees, showing higher specificity (SPE = 100 %) and reliability rate (RLR = 94.3 %).

Short-term Effects of Cadmium Exposure on Blood Pressure and Vascular Function in Wistar Rats.

Chronic cadmium exposure is known to be associated with vascular changes and increased blood pressure, but its short-term effects on the cardiovascular system remain poorly understood. This study aimed to investigate the pressoric and vascular effects of a 7-day exposure to CdCl2 in Wistar rats. The rats were divided in control group (Ct), which received tap water, and the Cd group, which received a 100 mg/L CdCl2 solution via drinking water for 7 days. We analyzed body weight, plasma Cadmium concentration, systolic blood pressure (SBP), and vascular responses. Despite relatively low plasma Cadmium concentration, the Cd group exhibited elevated SBP and increased contractile response to phenylephrine. Endothelium removal and NOS inhibition increased contractions in both groups. In the Cd group's aorta, we observed enhanced levels of phospho-eNOS (Ser1177) and basal NO release. Cd group showed reduced Catalase expression and increased basal release of H2O2, with catalase reducing the contractile response. In arteries pre-contracted with phenylephrine, Cd group showed impaired endothelium-dependent (Acetylcholine) and independent (sodium nitroprussiate-SNP) relaxation responses. However, responses to SNP were similar after pre-contraction with KCl in both groups. These data suggest early effects of Cadmium on blood pressure and aortic function, indicating impaired H2O2-scavenging by catalase. Increased H2O2 due to Cadmium exposure might explain heightened responses to phenylephrine and weakened relaxation responses mediated by the NO-K+-channels pathway. Our findings shed light on Cadmium's short-term impact on the cardiovascular system, providing insights into potential mechanisms underlying its effects on blood pressure regulation and vascular function.

Cessation Restores Blood Pressure Levels and Endothelial Function Affected by Cadmium Exposure on Rats.

Chronic cadmium exposure produces high blood pressure and endothelial damage; however, it is not known whether these effects could be reversed by interrupting the exposure to the metal. Therefore, we evaluate the systolic blood pressure (SBP) and vascular reactivity during and following chronic cadmium-exposure discontinuance. Rats received 100 mg.L-1 cadmium chloride (CdCl2) in the drinking water or tap water (Ct) for 30 days and/or tap water for 30 days more. The cadmium plasma content, blood pressure and vascular reactivity of isolated aorta were evaluated. Cadmium exposure increased cadmium plasma content, SBP and aorta contractile responses to phenylephrine, all reversed after suspending exposure. Endothelial removal and nitric oxide synthase (NOS) inhibition increased phenylephrine response both on control and Cd-discontinuation models. Cd-discontinuation group presented increased CAMKII and PKA protein expression, as peNOSSer1177. Superoxide dismutase (SOD) incubation reduced contractile response on control group, and catalase incubation enhanced the response to phenylephrine in this group. Meanwhile, both SOD2 and catalase protein expression were increased in Cd-cessation rats. Our findings provide evidence that increased SBP and endothelial dysfunction induced by Cd chronic exposure are reversed by suspending the metal exposure probably due to an improvement of antioxidant enzymes and eNOS function.

Sex-dependent vascular effects of cadmium sub-chronic exposure on rats.

Cadmium exposure is related to several cardiovascular diseases, such as hypertension, atherosclerosis and endothelial dysfunction. However, the toxic effect of cadmium can be dependent on the sex when examined sex in experimental models. The aim of this study was to analyze the effects of cadmium exposure on the cardiovascular system of male and female rodents. The experiments were carried out on both-sexes Wistar at 4 months of age, where from 3 months onwards, cadmium (CdCl2 100 mg/l in placed the drinking water for 30 days) or vehicle delivered (distilled water) was ingested. Before and after 30 days of exposure to cadmium, systolic blood pressure was regularly measured. After exposure, blood was collected to measure dosage of cadmium, in male and female, and estrogen in females. Vascular reactivity to phenylephrine (Phe), acetylcholine (ACh), and sodium nitroprusside (SNP) was studied at respective isolated aortic segments. After the period to Cd-exposure, systolic blood pressure was increased only in the male rats. Males also had higher levels of plasma cadmium than those of female rats, and exposure to the metal did not affect the amount of estrogen produced in the female rats. Increased myeloperoxidase (MPO) activity was also observed in both the males and females that had been exposed to the metal. Moreover, exposure to the cadmium reduced the ACh relaxation and increased vascular reactivity to Phe, resulting in an imbalance between nitric oxide superoxide anion in the isolated aorta of male rats. In female rats, sub-chronic cadmium exposure did not modify the vascular reactivity to Phe and neither to the ACh. The present study revealed that the Cd exposure for 30 days induced sex-dependent cardiovascular abnormalities.

The effects of drying methods and harvest season on piperine, essential oil composition, and multi-elemental composition of black pepper.

This study aimed to evaluate the piperine content, essential oil composition, and multi-elemental composition of black pepper samples according to different drying methods and harvest season. Differences in essential oil composition and B, Ca, K, Mg, and S were noted according to sampling campaign, indicating secondary metabolism plant alterations. Mechanical drying resulted in essential oil composition changes due to high temperature exposure during processing. Increases in Fe and Cr contents when employing mechanical dryers with direct heating were also observed, due to direct contact with metallic structures and particulate material from the burning process. The As and Pb contents of several samples were higher than the maximum permissible limits, reaching 0.46 and 0.56 mg kg-1, respectively, thus surpassing legislation safety limitations for human consumption.

The influence of beach geology and morphodynamics on chemical pollution assessments following a mining accident.

In the present study the distribution of chemical elements in beaches adjacent to the Doce River mouth hit by the tailings mud from a mining accident were assessed. Sedimentological and morphological coastal aspects were also considered. The results indicate that wave-exposed delta plain beaches exhibit high resiliency, despite their proximity to potential pollution sources. On the other hand, shore platform beaches tend to accumulate chemical elements, mainly due to limited cross-shore sediment exchanges. Arsenic concentrations in the evaluated shore platform beaches were significantly higher than the delta plain beach. Shore platform beaches are more susceptible to frequent flooding and to higher elemental concentrations at the berm and beach face. Thus, the morphological characteristics of the assessed shore platform beaches, and input from the mud plume must be considered in a joint assessment strategy in order to obtain a broad understanding of the actual scenario regarding beach contamination.

Moderate-intensity aerobic training reduces cardiac damage attributable to experimental iron overload in rats.

NEW FINDINGS: What is the central question of this study? The current literature indicates that oxidative stress plays a major role in iron overload. Although exercise is a well-established approach to treat/prevent cardiovascular diseases, its effects on iron overload are not known. What is the main finding and its importance? Moderate-intensity aerobic training had benefits in a rodent model of iron-overload cardiomyopathy by improving the antioxidant capacity of the heart. After further confirmation by translational and clinical studies, we should consider using this non-pharmacological, highly accessible and easily executable adjuvant approach allied to other therapies to improve the quality of life of iron-overloaded patients. ABSTRACT: Iron is an essential micronutrient for several life processes, but its excess can damage organs owing to oxidative stress, with cardiomyopathy being the leading cause of death in iron-overloaded patients. Although exercise has long been considered as a cardioprotective tool, its effects on iron overload are not known. This study was designed to investigate the effects of moderate-intensity aerobic training in rats previously submitted to chronic iron overload. Wistar rats received i.p. injections of iron dextran (100 mg/kg, 5 days/week for 4 weeks); thereafter, the rats were kept sedentary or exercised (60 min/day, progressive aerobic training, 60-70% of maximal speed, 5 days/week on a treadmill) for 8 weeks. At the end of the experimental period, haemodynamics were recorded and blood samples, livers and hearts harvested. Myocardial mechanics of papillary muscles were assessed in vitro, and cardiac remodelling was evaluated by histology and immunoblotting. Iron overload led to liver iron deposition, liver fibrosis and increased serum alanine aminotransferase and aspartate aminotransferase. Moreover, cardiac iron accumulation was accompanied by impaired myocardial mechanics, increased cardiac collagen type I and lipid peroxidation (TBARS), and release of creatine phosphokinase-MB to the serum. Although exercise did not influence iron levels, tissue injury markers were significantly reduced. Likewise, myocardial contractility and inotropic responsiveness were improved in exercised rats, in association with an increase in the endogenous antioxidant enzyme catalase. In conclusion, moderate-intensity aerobic exercise was associated with attenuated oxidative stress and cardiac damage in a rodent model of iron overload, thereby suggesting its potential role as a non-pharmacological adjuvant therapy for iron-overload cardiomyopathy.

Subacute cadmium exposure disrupts the hypothalamic-pituitary-gonadal axis, leading to polycystic ovarian syndrome and premature ovarian failure features in female rats.

Cadmium (Cd), a toxic heavy metal, is a known endocrine disruptor that is associated with reproductive complications. However, few studies have explored the effects of Cd exposure on features of polycystic ovary syndrome (PCOS) and premature ovary failure (POF). In this study, we assessed whether doses found in workers occupationally exposed to Cd and subacute exposure result in hypothalamic-pituitary-gonadal (HPG) axis and other irregularities. We administered CdCl2 to female rats (100 ppm in drinking water for 30 days) and then assessed Cd levels in the blood, HPG axis and uterus. Metabolic features, HPG axis function, reproductive tract (RT) morphophysiology, inflammation, oxidative stress (OS), and fibrosis were evaluated. Cd exposure increased Cd levels in the serum, HPG axis, and uterus. Cd rats displayed metabolic impairments, such as a reduction in adiposity, dyslipidemia, and insulin resistance (IR). Cd exposure also caused improper functioning in the HPG. Specifically, Cd exposure caused irregular estrous cyclicity, abnormal hypothalamic gene expression (upregulated - Kiss1, AR and mTOR; downregulated - Kiss1R, LepR and TNF-α), high LH levels, low AMH levels and abnormal ovarian follicular development, coupled with a reduction in ovarian reserve and antral follicle number was observed, suggesting ovarian depletion. Further, Cd exposure caused a reduction in corpora lutea (CL) and granulosa layer thickness together with an increase in cystic/atretic follicles. In addition, Cd exposure caused RT inflammation, OS and fibrosis. Finally, strong positive correlations were observed between serum, RT Cd levels, IR, dyslipidemia and estrous cycle length, cystic, atretic follicles, LH levels, and RT inflammation. Thus, these data suggest that subacute Cd exposure using doses found in workers occupationally exposed to Cd disrupt the HPG axis function, leading to PCOS and POF features and other abnormalities in female rats.

Chronic iron overload induces vascular dysfunction in resistance pulmonary arteries associated with right ventricular remodeling in rats.

Although iron excess is toxic to the vasculature and even that pulmonary hypertension has been reported in this scenario, the role of iron overload per se remains to be clarified. This study aimed to test the effects of chronic iron-overload in rats on the morphophysiology of resistance pulmonary arteries (RPA) and right ventricle (RV) remodeling. Rats were injected with saline or iron-dextran (10, 100 and 200 mg/kg/day i.p.) for 28 days. Our results indicated increased circulating iron with significant lung deposits. Moreover, rats treated with the highest dose exhibited RV dysfunction and hypertrophy; inward remodeling and increased vasoconstriction of the RPA. Vascular hyperreactivity was accompanied by reduced nitric oxide (NO), and was reversed by incubation with Dimethylsulfoxide, Catalase and Tempol. The NADPH oxidase subunit gp91phox was increased due to iron-overload, and incubation with angiotensin II type-1 receptor (AT1) antagonist losartan not only reduced oxidative stress but also restored vascular function. Thus, we concluded that AT1 pathway plays a role in pulmonary vascular dysfunction by increasing oxidative stress and reducing NO bioavailability, thereby contributing to vascular remodeling and pulmonary hypertension of iron-overload. This finding should instigate future studies on the beneficial impacts of in vivo blockade of AT1 receptor under iron overload.