J Physiol Biochem. 2011; 67(3):339-349. PMID: 21336648

Abstract Recent studies have shown that lead (Pb) could disrupt tissue prooxidant/antioxidant balance which lead to physiological dysfunction. Natural antioxidants are particularly useful in such situation. Current study was designed to investigate efficacy of green tea extract (GTE), on oxidative status in brain tissue and blood caused by chronic oral Pb administration in rats. Four groups of adult male rats (each 15 rats) were utilized: control group; GTE-group (oral 1.5% w/v GTE for 6 weeks); Pb-group (oral 0.4% lead acetate for 6 weeks), and Pb+GTE-group (1.5% GTE and 0.4% lead acetate for 6 weeks). Levels of prooxidant/antioxidant parameters [lipid peroxides (LPO), nitric oxides (NO), total antioxidant capacity (TAC), glutathione (GSH), glutathione-S-transferase (GST), superoxide dismutase (SOD)] in plasma, erythrocytes, and brain tissue homogenate were measured using colorimetric methods. Pb concentrations in whole blood and brain tissue homogenate were measured by atomic absorption. In Pb-group, levels of LPO were higher while NO and GSH were lower in plasma, erythrocytes, and brain tissue than controls. TAC in plasma, SOD in erythrocytes, and GST in brain tissue homogenate were lower in Pb-group versus control. GTE co-administrated with Pb-reduced Pb contents, increased antioxidant status than Pb-group. In erythrocytes, Pb correlated positively with LPO and negatively with NO, GSH, SOD, and Hb. In brain tissue homogenate, Pb correlated positively with LPO and negatively with GSH. This study suggests that lead induce toxicity by interfering balance between prooxidant/antioxidant. Treatment of rats with GTE combined with Pb enhances antioxidant/ detoxification system which reduced oxidative stress. These observations suggest that GTE is a potential complementary agent in treatment of chronic lead intoxication. Keywords Rat . Brain tissue homogenate . Erythrocyte . Lead toxicity. Green tea extract . Oxidative stress

Abstract

This work aims at determining the difference of pro-inflammatory cytokines, adhesion molecules in a synovial fluid, serum of rheumatoid arthritis, osteoarthritis patients. Synovial fluid and serum were obtained from rheumatoid arthritis (n=21), osteoarthritis (n=11) patients, serum of healthy individuals (n=12). Interleukin-1β, tumor necrosis factor-alpha, sE-selectin levels were measured by Enzyme-Linked Immunosorbent Assay Test. Compared to controls, S-sE-selectin was significantly elevated in rheumatoid arthritis while S-IL-1β, S-TNF-α were elevated in rheumatoid arthritis and osteoarthritis patients. S-sE-selectin, SF-IL-1β, and SF-TNF-α were significantly elevated in rheumatoid arthritis versus osteoarthritis. In rheumatoid arthritis, SF-sE-selectin was significantly lower while SF-TNF-α was higher than serum in rheumatoid arthritis and osteoarthritis. In rheumatoid arthritis, positive correlation between SF-E-selectin with serum C-reactive Protein and S-sE-selectin; between S-sE-selectin with disease duration and S-TNF-α between S-IL1-β with SF-IL1-β and disease activity while the negative correlation between S-TNF-α with grip strength were found. A degree of vascular endothelial activation reflected by increased sE-selectin is associated with disease activity, duration in rheumatoid arthritis. The positive association between IL-1β, disease activity and a negative association between TNF-α, grip strength indicated that serial estimation of these cytokines may be used to monitor disease progression. Elevated TNF-α in synovial fluid than in serum of rheumatoid arthritis, osteoarthritis patients indicates its local formation in the synovium.

Abstract Background Afatoxin B (AFB) induces toxicological efects on the liver and immune organs. The whey proteins can modulate the immune response during afatoxicosis. Our work evaluates the novel polylactic acid-glycolic acid-chitosanencapsulated bovine and camel whey proteins against AFB-induced thymic and splenic atrophy in rats. Methods and results Seventy adult male Wister albino rats were divided into a control healthy group (G1) and six AFB1- intoxicated groups (G2–G7). One of the following supplements: distilled water, camel whey proteins (CWP), bovine whey proteins, poly (d, l-lactide-co-glycolide) (PLGA)- chitosan-loaded with camel whey protein microparticles (CMP), PLGAchitosan loaded with bovine whey protein microparticles (BMP), and PLGA-chitosan nanoparticles were administered as prophylactic supplements to AFB1-intoxicated groups. The AFB-treated group showed signifcantly higher hepatic levels of oxidative stress and lower levels of antioxidants. In the afatoxicated group, atrophy of the splenic lymphatic nodules and disfgurement in the organisation with an apparent decrease in the thickness of the cortex in the thymus were observed, as well as a decrease in splenic and thymic CD4+T and CD8+T lymphocytes. Moreover, CXCL12 levels were downregulated, whereas tumour necrosis factor-alpha, nuclear factor kappa B, and cleaved caspase-3 levels were upregulated. CWP, BMP, and CMP supplements markedly decreased oxidative stress, infammation, and apoptosis, as well as signifcantly raised CXCL12, CD4+T, and CD8+T cells. Conclusions The CWP, BMP, and CMP supplements rescue the liver and immune tissues from the toxic efects of AFB through their antioxidant, antiapoptotic, anti-infammatory, and chemotaxis-enhancing roles.