The immune modulatory role of marjoram extract on imidacloprid induced toxic effects in thymus and spleen of adult rats.

Imidacloprid (IMID), one of environmental persistent neonicotinoid insecticides, has been used a long time ago and categorized from insecticide induced moderate toxicity by World Health Organization (WHO). Marjoram, is one of the most worldwide used herbs in Egypt due to its antioxidant, anti-inflammatory, anti-genotoxic, anti-mutagenic, anticoagulant, and beneficial effects. This study aimed to evaluate the protective role of marjoram extract on the immunotoxic response and oxidative stress induced by IMID in the immune lymphoid organs (thymus and spleen) of rats. Fifty adult male albino rats were divided randomly into five groups; negative and positive (distilled water) control, marjoram extract (200 mg/kg/day), IMID (22.5 mg/kg/day), marjoram extract + IMID (200 mg/kg +22.5 mg/kg) orally for 8 weeks. Marjoram pretreatment reversed reduced animals body, thymus and spleen weights attributed to IMID. It amended the significantly elevated total leukocytes, neutrophils percentage, increased immunoglobulin G and the significantly reduction of lymphocytes percentage, phagocytic activity, phagocytic index and lysozyme activity induced by IMID. Moreover, marjoram administration significantly reduced thymic and splenic gene expression of interleukin-1ß, interleukin-6, tumor necrosis factor-α and increased interleukin-10, in addition, it decreased thymic and splenic contents of malondialdehyde and restored the reduced antioxidant enzymes' activities following IMID exposure. Marjoram ameliorated IMID induced histopathological alterations in thymus and spleen and adjusted IMID immunomodulatory effects by increased the downregulation of CD4 and CD8 immune reactive cell expression. Conclusion, Marjoram has a protective role to reverse IMID immune toxic effects in thymus and spleen tissues of rats by its antioxidant, anti-inflammatory and immunomodulatory defense mechanisms.

Combined lead and zinc oxide-nanoparticles induced thyroid toxicity through 8-OHdG oxidative stress-mediated inflammation, apoptosis, and Nrf2 activation in rats.

A human is exposed to a chemical mixture rather than a single chemical, particularly with the wide spread of nanomaterials. Therefore, the present study evaluated the combined exposure of lead acetate (Pb) and zinc oxide-nanoparticles (ZnO-NPs) compared to each metal alone on the thyroid gland of adult rats. A total of 30 adult male albino rats were divided into four groups, group I (control), group II received Pb (10 mg/kg), group III received ZnO-NPs (85 mg/kg) and group IV co-administrated the two metals in the same previous doses. The materials were gavaged for 8 weeks. The toxicity was assessed through several biochemical parameters. Our results revealed significant body weight reduction relative to increased thyroid weights, decreased both of serum-free triiodothyronine (FT3), tetra-iodothyronine (FT4), increased thyroid-stimulating hormone (TSH), increased serum and thyroid levels of Pb and zinc, significant elevation in tumor necrosis factor-α (TNF-α), reduction in interleukin 4 (IL4), upregulation of Bax, and downregulation of Bcl-2 genes. Additionally, there was significant overexpression of nuclear factor erythroid 2-related factor 2(Nrf2), 8-Hydroxydeoxyguanosine(8-OHdG), the elevation of tissues malondialdehyde (MDA), reduction of tissues total antioxidant capacity (TAC), and disruptive thyroid structural alterations in all metals groups with marked changes in the combined metals group. In conclusion, the combined exposure of Pb and ZnO-NPs induced pronounced toxic thyroid injury, pointing to additive effects in rats than the individual metal effects through different significant changes of disruptive thyroid structural alterations related to the loading of thyroid tissues with Pb and zinc metals producing oxidative stress that mediated inflammation and apoptosis.

Ameliorating Iron Overload in Intestinal Tissue of Adult Male Rats: Quercetin vs Deferoxamine.

OBJECTIVE: The aim of our study is to compare the role of the new natural alternative (Quercetin) with the current iron-chelation therapy (Deferoxamine (DFO)) in the effect of iron overload on small intestinal tissues and to investigate the possible underlying molecular mechanisms of such toxicity. METHODS: Forty-two adult male albino rats were divided into six groups: control groups, DFO, Quercetin, iron overload, iron overload+DFO, and iron overload+Quercetin groups. Animals received daily intraperitoneal injection of Deferoxamine (125 mg /kg), Quercetin (10 mg/kg), and ferric dextran (200 mg/kg) for 2 weeks. RESULTS: Iron overloaded group showed significant increase in serum iron, total iron binding capacity (TIBC), transferrin saturation percentage (TS %) hepcidin (HEPC), serum ferritin, nontransferrin bound iron (NTBI), and small intestinal tissues iron levels. Iron overload significantly increased the serum oxidative stress indicator (MDA) and reduced serum total antioxidant capacity (TAC). On the other hand, iron overload increased IL6 and reduced IL10 in small intestinal tissues reflecting inflammatory condition and increased caspase 3 reactivity indicating apoptosis and increased iNOs expressing cell indicting oxidative stress especially in ileum. In addition, it induced small intestinal tissues pathological alterations. The treatment with Quercetin showed nonsignificant differences as compared to treatment with DFO that chelated the serum and tissue iron and improved the oxidative stress and reduced tissue IL6 and increased IL10 and decreased caspase 3 and iNOs expressing cells in small intestinal tissues. Moreover, it ameliorated the iron overload induced pathological alterations. CONCLUSION: Our study showed the potential role of Quercetin as iron chelator like DFO in case of iron overload induced small intestinal toxicity in adult rats because of its serum and tissue iron chelation, improvement of serum, and small intestinal oxidative stress, ameliorating iron induced intestinal inflammation, apoptosis, and histopathological alterations.