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.

Zinc nanoparticles ameliorate oxidative stress and apoptosis induced by silver nanoparticles in the brain of male rats.

The current study was conducted to investigate the possible ameliorative role of zinc nanoparticles (Zn NPs) against silver nanoparticles (Ag NPs)-induced oxidative and apoptotic brain damage in adult male rats. Twenty-four mature Wistar rats were randomly and equally divided into four groups: control group, Ag NPs group, Zn NPs group, and Ag NPs + Zn NPs group. Rats were exposed to Ag NPs (50 mg/kg) and/or Zn NPs (30 mg/kg) daily by oral gavage for 12 weeks. The results revealed that exposure to Ag NPs significantly increased malondialdehyde (MDA) content, decreased catalase and reduced glutathione (GSH) activities, downregulated the relative mRNA expression of antioxidant-related genes (Nrf-2 and SOD), and upregulated the relative mRNA expression of apoptosis-related genes (Bax, caspase 3 and caspase 9) in the brain tissue. Furthermore, severe neuropathological lesions with a substantial increase in the caspase 3 and glial fibrillary acidic protein (GFAP) immunoreactivity were observed in the cerebrum and cerebellum of Ag NPs-exposed rats. Conversely, co-administration of Zn NPs with Ag NPs significantly ameliorated most of these neurotoxic effects. Collectively, Zn NPs can be used as a potent prophylactic agent against Ag NPs-induced oxidative and apoptotic neural damage.

Evaluation of the Ameliorative Effect of Zinc Nanoparticles against Silver Nanoparticle-Induced Toxicity in Liver and Kidney of Rats.

Silver nanoparticles (Ag-NPs) have various pharmaceutical and biomedical applications owing to their unique physicochemical properties. Zinc (Zn) is an essential trace element, a strong antioxidant, and has a primary role in gene expression, enzymatic reactions, and protein synthesis. The present study aims to explore the toxic effects of Ag-NPs (50 nm) on the liver and kidney of rats and also to evaluate the potential protective effect of Zn-NPs (100 nm) against these adverse effects. Forty adult Sprague-Dawley rats were randomly divided into four equal groups: control group, Ag-NPs group, Zn-NPs group, and Ag-NPs + Zn-NPs group. Ag-NPs (50 mg/kg) and/or Zn-NPs (30 mg/kg) were administered daily by gavage for 90 days. The results showed that exposure to Ag-NPs increased serum ALT, AST, urea, and creatinine. Ag-NPs also induced oxidative stress and lipid peroxidation and increased inflammatory cytokines in hepatic and renal tissues. Moreover, histopathological and immunohistochemical examinations revealed various histological alterations and positive caspase-3 expressions in the liver and kidney following exposure to Ag-NPs. On the other hand, most of these toxic effects were ameliorated by co-administration of Zn-NPs. It was concluded that Ag-NPs have hepatotoxic and nephrotoxic effects in rats via different mechanisms including oxidative stress, inflammation, and apoptosis and that Zn-NPs can be used to alleviate these harmful effects by their antioxidative, anti-inflammatory, and antiapoptotic properties.

Zinc Nanoparticles Ameliorate the Reproductive Toxicity Induced by Silver Nanoparticles in Male Rats.

INTRODUCTION: Silver nanoparticles (Ag-NPs) are among the most commonly used nanoparticles in different fields. Zinc nanoparticles (Zn-NPs) are known for their antioxidant effect. This study was designed to investigate the adverse effects of Ag-NPs (50 nm) on the male reproductive system and also the ameliorative effect of Zn-NPs (100 nm) against these harmful effects. METHODS: Forty adult male rats were used in this study; they were randomly divided into four equal groups: control group, Ag-NPs group, Zn-NPs group, Ag-NPs + Zn-NPs group. Ag-NPs (50 mg/kg) and/or Zn-NPs (30 mg/kg) were administered orally for 90 days. RESULTS: The results revealed that exposure to Ag-NPs adversely affected sperm motility, morphology, viability, and concentration. Ag-NPs also induced oxidative stress and lipid peroxidation in testicular tissue. The exposure to Ag-NPs decreased serum FSH, LH, and testosterone hormones. Additionally, comet assay revealed DNA degeneration in the testicular tissue of rats exposed to Ag-NPs. Histopathological examination showed various histological alterations in the testes of rats intoxicated with Ag-NPs. Furthermore, co-administration of Zn-NPs ameliorated most of the toxic effects of Ag-NPs via their antioxidative capacity.

Nanoparticles of zinc oxide defeat chlorpyrifos-induced immunotoxic effects and histopathological alterations.

BACKGROUND AND AIM: Chlorpyrifos (CPF) is a widely used organophosphate insecticide. Nanoparticles of zinc oxide (ZnO NPs) physically showed effective adsorbing property for some insecticides. The study was conducted to estimate the potential effect of ZnO NPs against CPF toxicity. MATERIALS AND METHODS: Four groups of male rats were used; control group and three groups received drinking water contained 75 mg/L CPF, combined 75 mg/L CPF and 200 mg/L ZnO NPs, and 200 mg/L ZnO NPs, respectively. RESULTS: CPF significantly decreased macrophage activity, serum lysozyme activity, and levels of interleukin-2 (IL-2) and IL-6; increased the percentage of DNA degeneration on comet assay of lymphocytes and significantly elevated hepatic and splenic malondialdehyde contents; and decreased their glutathione contents. The liver and spleen showed marked histological alterations after exposure to CPF with decreased expression of acetylcholinesterase. The coadministration of ZnO NPs ameliorated most of the undesirable effects of CPF, through elevation of macrophage and serum lysozyme activities, increased the levels of IL-2 and IL-6, corrected the oxidative stress markers, and alleviated most of the adverse effect exerted by CPF in liver and spleen tissues. CONCLUSION: The addition of ZnO NPs to CPF-contaminated drinking water may be useful as a powerful antioxidant agent against toxic damage induced by CPF particularly in individuals who are on daily occupational exposure to low doses of CPF.

Modulating effect of MgO-SiO2 nanoparticles on immunological and histopathological alterations induced by aflatoxicosis in rats.

INTRODUCTION: AflatoxinB1 (AFB1) is well-known as a feed borne-hepatotoxic and immunosuppressive mycotoxin. This study was conducted to evaluate the efficacy of nanocomposite magnesium oxide and silicon oxide (MgO-SiO2) in reducing the toxic effects of AFB1on the immunity and histological alterations in liver, spleen and intestine of adult male rats. EXPERIMENTAL DESIGN: Animals were divided into a control (Gp1) and three experimental groups (Gps); Gp2 received feed contained 200 ppb AFB1, Gp3 received feed contained 200 ppb AFB1 and 0.5 g/kg MgO-SiO2 nanocomposite. While, rats of Gp4 received feed contained 0.5 g/kg MgO-SiO2 nano-composite. METHODS: Cellular and humoral immune responses, as well as histopathological examination and caspase-3 expression in liver, spleen, and intestine, were all evaluated. Residual concentration of AFB1was determined in serum, liver and fecal samples. The obtained data were statistically analyzed. RESULTS: AFB1markedly reduced body weight gain and food and water consumption. Cellular immune response (total and differential leukocytes count, neutrophils' phagocytic activity, lymphocyte transformation, macrophage activity and serum lysozyme activity), serum total protein, and humoral immune response (fractions of protein as estimated by SDS- PAGE electrophoresis) were all severely reduced by AFB1. Moreover, AFB1induced marked histological alterations and apoptosis in liver, spleen, and intestine. CONCLUSION: These findings suggested that the nanocomposite MgO-SiO2 has high affinity to adsorb AFB1 and can effectively modulate its toxicity in rats. IMPACT STATEMENT: Nanocomposite MgO-SiO2 may offer a novel effective and cheap approach for the preventive management of aflatoxicosis in animals.