Trace Elements Homeostatic Imbalance in Psoriasis: a Meta-Analysis Abstract Studies point out that trace elements take vital roles in immunological and inflammatory reactions, such as psoriasis, while the conclusions are controversial. The purpose of this study was to analyze the existing literatures and explore the relationship between the risk of psoriasis and four trace elements zinc (Zn), copper (Cu), iron (Fe), and selenium (Se). We identified 42 studies through the databases PubMed, Embase, Cochrane Library, Google Scholar, and Web of knowledge. After the meta-analysis, the serum zinc, iron, and selenium levels showed no remarkable difference between psoriasis and controls. The people with psoriasis showed a higher level of zinc in lesion tissue (standard mean difference (SMD) = 14.43; 95% confidence interval (CI), 7.89–20.97; P < 0.0001), and a higher level of serum copper than controls (SMD = 18.23; 95% CI, 5.06–31.40; P = 0.007). Our findings indicated that the trace element of copper and zinc levels are in a homeostatic imbalance in psoriasis patients when compared with controls, which raise the question whether this imbalance can be taken as the therapy target for psoriasis.

Dietary Intake of Cadmium, Chromium, Copper, Nickel, and Lead through the Consumption of Meat, Liver, and Kidney and Assessment of Human Health Risk in Birjand, Southeast of Iran Abstract This study aimed to evaluate the mean concentration of cadmium (Cd), chromium (Cr), copper (Cu), nickel (Ni), and lead (Pb) in the meat and offal of cow and sheep. Also, the estimated daily intake (EDI) and health risk of these metals were calculated. Analysis of metals was undertaken by the use of an inductively coupled plasma-optic emission spectroscopy (ICP-OES). All samples were contaminated with all metals. Principal component analysis (PCA) showed a clear differentiation of cow and sheep in both the kidney and liver samples. In the liver and kidney, level of Cd, Cu, and Pb were positively correlated. The highest target hazard quotients (THQs) were calculated for Pb. Cd level in cow kidney had the highest carcinogenic rate (CR). Although, hazard index (HI) was lower than one, consumption of muscle especially in children should be noticed in both national and international consumers due to higher level of HI.

Comparison of Copper Concentration Between Rejected Renal Grafts and Cancerous Kidneys Abstract In the body, disorders in the composition and concentration of trace elements, including copper, can lead to the development of various alterations that may result in incorrect functioning of the kidneys. Data on the concentrations of copper in human kidneys are discussed; however, little is known about the concentration of trace elements within rejected renal grafts and kidneys with tumor lesions. The aim of our study was to compare the copper concentration between cancerous kidneys and rejected renal grafts with the division on renal cortex and renal medulla. Material consisted of kidneys from patients hospitalized at the Department of Urology and General Surgery and Transplantation of the Independent Public Clinical Hospital No. 2 at the Pomeranian Medical University in Szczecin, north-western Poland. The study material consisted of kidneys with tumor lesions (n = 33), and renal grafts (n = 10), obtained from patients belongs to the north-western areas of Poland. The examination was performed using ICP-AES method. Regarding the pathological kidneys, excluding grafts, the concentration of Cu in the renal cortex was 52% higher than in medullary region and the difference between the compared concentrations was statistically confirmed (p < 0.05). Taking into account renal grafts, the concentration of Cu in the medulla was slightly lower than in the cortex (less than 3%). In summary, copper in rejected and cancerous kidneys tends to accumulate in higher amount in the renal cortex than medulla, what can be explained by the fact that renal corpuscles, where the first phase of filtration is performed, are located only in the cortical region of the kidney. Furthermore, renal grafts accumulate significantly less copper than kidneys with neoplastic changes, what could have been caused by immunosuppressive medicines used by the graft recipients. The lower copper concentration in renal grafts could be a consequence of the altered immune system, including inflammatory process or/and non-immune mechanisms. Additionally, cancerous and non-cancerous kidneys exhibit different perfusion rate in renal glomeruli, what can finally lead to disparity in chemical elements concentration, including copper.

Pharmacokinetics of Selenium in Healthy Piglets After Different Routes of Administration: Application of Pharmacokinetic Data to the Risk Assessment of Selenium Abstract Selenium (Se) is a trace element in the environment. Although it is a necessary trace element for human and animal health, excessive Se can also pollute the environment and show toxic effects on humans and animals. Since the safe dose range of Se is narrow, it is important to study the pharmacokinetics of Se in order to make better use of the biological effects of Se. In the present study, we investigated the pharmacokinetic process of sodium selenate in healthy piglet plasma after either intramuscular injection or oral administrations, and examined dynamic changes of antioxidant system in healthy piglets after Se supplementation. The results showed that the Se reached the peak concentration of (0.2451 ± 0.0123) μg mL−1 at (0.4237 ± 0.0185) h following intramuscular injection administration and (0.1781 ± 0.0142) μg mL−1 at (2.1517 ± 0.1806) h following oral administration in the plasma. The average AUC of sodium selenite following intramuscular injection and oral administrations was (31.7260 ± 1.3574) and (75.1460 ± 3.4127) mg L−1 h−1, respectively. Total antioxidant capacity (T-AOC), glutathione peroxidase (GPx), and superoxide dismutase (SOD) generally show an upward trend and malondialdehyde (MDA) shows a downward trend, regardless of intramuscular injection or oral sodium selenite. An increased concentration of Se was observed in the serum of healthy piglets after intramuscular injection and oral sodium selenite. Our results indicated that the pharmacokinetic process of sodium selenate in healthy piglet blood conforms to the two-chamber open model. Its pharmacokinetic properties are rapid absorption and slow excretion. Antioxidant systems in healthy piglets vary with Se levels, but there is a significant lag period compared with the latter. Our current findings will provide a more complete understanding of clinical rational Se supplementation and avoid contamination of the environment by overdose.

Role of Oxidative Stress in Lithium-Induced Nephropathy Abstract Long-term lithium treatment was associated with chronic kidney disease and renal failure although the underlying pathogenic mechanisms are not certainty known. The aim of this study was to evaluate changes in oxidative stress measures as well as renal functional and structural alterations associated with chronic use of lithium in rats. Forty Wistar male rats were randomized into four groups: control groups fed ad libitum powered standard diet for 1 and 3 months and experimental groups fed ad libitum the same diet supplemented with 60 mmol/kg diet for 1 and 3 months. Histopathological changes, laboratory parameters, and oxidative stress measurements were assessed at months 1 and 3. The experimental animals showed alteration of the cortical tubules from the first month of lithium-treatment and a decrease in the glomerular filtration rate and in the glomerular area at the third month. There was an increase in thiobarbituric acid reactive substances and carbonyls, as well as an increase in reduced glutathione, in the kidney of rats exposed to lithium. These changes were evident from the first month of treatment and remained throughout the experiment. Our results suggest that, oxidative stress could be one of the pathogenic mechanisms involved in the structural and functional alterations of the kidney associated with prolonged use of lithium. The study of the pathogenic mechanisms involved in lithium-induced nephropathy is a critical issue for the development of new strategies for prevention and/or early detection.

Zinc Deficiency and Arsenic Exposure Can Act Both Independently or Cooperatively to Affect Zinc Status, Oxidative Stress, and Inflammatory Response Abstract The negative health impact of zinc deficiency overlaps significantly with arsenic exposure, and is associated with increased risk for chronic diseases. Arsenic contamination in the groundwater often co-exists in regions of the world that are prone to zinc deficiency. Notably, low zinc status shares many hallmarks of arsenic exposure, including increased oxidative stress and inflammation. Despite their common targets and frequent co-distribution in the population, little is known regarding the interaction between zinc deficiency and arsenic exposure. In this study, we tested the effect of arsenic exposure at environmentally relevant doses in combination with a physiologically relevant level of zinc deficiency (marginal zinc deficiency) on zinc status, oxidative damage, and inflammation. In cell culture, zinc-deficient THP-1 monocytes co-exposed with arsenic resulted in further reduction in intracellular zinc, as well as further increase in oxidative stress and inflammatory markers. In an animal study, zinc-deficient mice had further decrease in zinc status when co-exposed to arsenic. Zinc deficiency, but not arsenic exposure, resulted in an increase in baseline transcript abundance of inflammatory markers in the liver. Upon lipopolysaccharide challenge to elicit an acute inflammatory response, arsenic exposure, but not zinc deficiency, resulted in an increase in proinflammatory response. In summary, zinc deficiency and arsenic exposure can function independently or cooperatively to affect zinc status, oxidant stress, and proinflammatory response. The results highlight the need to consider both nutritional status and arsenic exposures together when considering their impact on health outcomes in susceptible populations.

The Inverted U-Curve Association of Fluoride and Osteoclast Formation in Mice Abstract The effect of fluoride on osteoclasts is still controversial. In the past, researchers thought that the effects of fluoride on osteoclast and osteoblast formation occurred in a dose-dependent pattern. However, our previous in vitro study showed fluoride elicited a notably different effect on osteoclast formation. To further verify the relationship between fluoride and osteoclast formation in vivo, 60 male C57BL/6 mice were randomly divided into three groups: two treatment groups consuming water supplemented with 50 and 100 mg/L of fluoride, and a third control group with nonsupplemented water. Ion selective electrode method analysis was used to detect bone fluoride content, and the effects of fluoride on bone tissue were assessed with hematoxylin and eosin (HE) staining. Additionally, the expression of BGP and ALP were examined by Western blot analysis, and tartrate-resistant acid phosphatase (TRAP) was assessed with immunohistochemistry. Osteoclasts in bone tissue were identified with a combination method of TRAP staining and cell morphology assessment. Results showed increasing expression of BGP among treatment groups as fluoride exposure increased, and ALP expression in the 100 mg/L treatment group was significantly higher than that for both the 50 mg/L treatment and control groups. The number of osteoclasts in the 50 mg/L group was highest amongst the three groups, followed by the 100 mg/L treatment and then by the control group, with the latter showing significantly fewer osteoclasts than in either treatment group. These results suggest that fluoride enhances bone formation at increasing levels of fluoride exposure. However, the inverted U-curve association was found between fluoride exposure and osteoclast formation, with the higher dose of fluoride having slightly reduced osteoclast formation. The results from this study may provide key insights towards understanding the role of osteoclasts in the progression of skeletal fluorosis.

Association Between Cortisol, Insulin Resistance and Zinc in Obesity: a Mini-Review Abstract Adipose tissue is considered an endocrine organ and its excess compromises the immune response and the metabolism of hormones and nutrients. Furthermore, visceral fat accumulation contributes to increased cortisol synthesis, which in turn induces metallothionein and Zip14 expression, which are proteins that contribute to reducing plasma zinc levels. Zinc plays a critical role in the secretion and signaling of insulin. Changes in the biochemical parameters of zinc, as observed in individuals who are obese, contribute to the manifestation of related disorders such as insulin resistance. Thus, the purpose of this review is to provide an update on the current information on the relationship between cortisol, zinc, and insulin resistance in obesity. The data in the literature provide evidence that cortisol affects zinc metabolism, and indicate possible repercussions on insulin signaling that might contribute to the development of resistance to the actions of insulin in obesity.

Protective Effects of Salidroside on Lead Acetate-induced Oxidative Stress and Hepatotoxicity in Sprague-Dawley Rats Abstract Lead has heavy metal toxicity which endangers human and animal health. Salidroside (SDS) is a natural antioxidant that has extensive pharmacological usage. However, its protective effects on lead-induced oxidative stress and hepatotoxicity has not been reported. In this study, we established an animal model to evaluate the protective effects of SDS on chronic lead exposure induced oxidative stress and hepatotoxicity. Forty healthy Sprague-Dawley (SD) rats were assigned to control group (control, animals were provided with distilled water, n = 10); lead acetate-exposed group (PbAc, animals received lead acetate solution of 500 ppm for 60 days, n = 10); low dosage of SDS-treated group (PbAc-SDS-L, lead acetate exposed animals were given intragastric SDS 150 mg/kg body weight for 60 days, n = 10); and high dosage of SDS-treated group (PbAc-SDS-H, lead acetate exposed animals were given intragastric SDS 300 mg/kg body weight for 60 days, n = 10). The results showed that lead exposure caused a significant increase in serum ALP, AST, ALT, and TB (P < 0.01), and these were reversed after treatment with salidroside for 60 days. Compared to the control, the liver GSH, SOD, and GSH-Px were decreased significantly after lead acetate exposure (P < 0.01). However, after treatment with SDS for 60 days, those were dose-dependently reversed. Similarly, MDA was significantly increased in the PbAc group (P < 0.01), and it was significantly decreased in SDS treatment group. Moreover, SDS ameliorated lead-induced congestion and necrosis of hepatocytes. In addition, the RT-PCR and immunohistochemistry results revealed that the PbAc group showed a significant increase in the protein and mRNA of cytochrome P450 2E1 (CYP2E1) and NADPH oxidase 2 (NOX2) in rat liver. Treatment with SDS significantly reversed CYP2E1 and NOX2 expressions in the liver of lead-exposed rats. The results above indicated that SDS has obvious antioxidant activity; it can cure liver injury caused by lead acetate by inhibiting oxidative stress and increasing the antioxidant stress activity, thus improving the liver tissue structure.

Effects of Fungal Polysaccharide on Oxidative Damage and TLR4 Pathway to the Central Immune Organs in Cadmium Intoxication in Chickens Abstract Cadmium (Cd) can cause animal organism damage, but there have been few studies on the damage of cadmium to the immune organs of birds. Most fungal polysaccharide has antioxidant and immunomodulatory effects. The experimental study investigated the effects of fungal polysaccharide (Agaricus blazei Murill polysaccharide and Ganoderma luciduccharide) on the oxidative damage of central immune organs (thymus and bursa of Fabricius) and on the Toll-like receptor 4 (TLR4) pathway in cadmium-poisoned chickens. The results showed that Agaricus blazei polysaccharide and Ganoderma lucidum polysaccharide can reduce cadmium content, TLR4 expression, inflammatory factor (IL-1β, IL-6, TNF-α) content, and lipid peroxidation product MDA content and increase the activity of antioxidant enzymes SOD and GSH-Px in thymus and bursa of cadmium poisoning chickens. Ganoderma lucidum polysaccharide could decrease the expression of TLR4, IL-1β, and IL-6 in cadmium poisoning peripheral blood lymphocytes of chicken, and TLR4 inhibitor had the same effect. The results demonstrated the protective effects of Agaricus blazei Murill polysaccharide and Ganoderma lucidum polysaccharides on the damage of the central immune organs of chickens caused by cadmium poisoning were closely related to the TLR4 signaling pathway and oxidative stress.