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Gustavo F Gonzales - One of the best experts on this subject based on the ideXlab platform.

  • lepidium meyenii maca reversed the Lead Acetate induced damage on reproductive function in male rats
    Food and Chemical Toxicology, 2006
    Co-Authors: Julio Rubio, Marissa I Riqueros, Manuel Gasco, Sandra Yucra, Sara Miranda, Gustavo F Gonzales
    Abstract:

    Abstract Rats were treated with 0, 8, 16 and 24 mg/kg of Lead Acetate (LA) (i.p.) for 35 days with or without Maca. Maca was co-administrated orally from day 18 to day 35. The lengths of stages of the seminiferous epithelium were assessed by transillumination. Also, sex organ weights, testicular and epididymal sperm count, sperm motility, daily sperm production, sperm transit rate and serum testosterone levels were measured. Lead Acetate treatment resulted in a dose–response reduction of lengths of stages VIII and IX–XI, and serum testosterone levels. However, rats treated with 8 and 16 mg/kg but not 24 mg/kg of Lead Acetate showed a low number of testicular spermatids, low daily sperm production (DSP) and low epididymal sperm count. Administration of Maca to rats treated with Lead Acetate resulted in higher lengths of stages VIII and IX–XI with respect to Lead Acetate-treated rats. Moreover, treatment with Maca to Lead Acetate-treated rats resulted in lengths of stages VIII and IX–XI similar to the control group. Maca administration also reduced the deleterious effect on DSP caused by Lead Acetate treatment. Maca prevented LA-induced spermatogenic disruption in rats and it may become in a potential treatment of male infertility associated with Lead exposure.

Julio Rubio - One of the best experts on this subject based on the ideXlab platform.

  • lepidium meyenii maca reversed the Lead Acetate induced damage on reproductive function in male rats
    Food and Chemical Toxicology, 2006
    Co-Authors: Julio Rubio, Marissa I Riqueros, Manuel Gasco, Sandra Yucra, Sara Miranda, Gustavo F Gonzales
    Abstract:

    Abstract Rats were treated with 0, 8, 16 and 24 mg/kg of Lead Acetate (LA) (i.p.) for 35 days with or without Maca. Maca was co-administrated orally from day 18 to day 35. The lengths of stages of the seminiferous epithelium were assessed by transillumination. Also, sex organ weights, testicular and epididymal sperm count, sperm motility, daily sperm production, sperm transit rate and serum testosterone levels were measured. Lead Acetate treatment resulted in a dose–response reduction of lengths of stages VIII and IX–XI, and serum testosterone levels. However, rats treated with 8 and 16 mg/kg but not 24 mg/kg of Lead Acetate showed a low number of testicular spermatids, low daily sperm production (DSP) and low epididymal sperm count. Administration of Maca to rats treated with Lead Acetate resulted in higher lengths of stages VIII and IX–XI with respect to Lead Acetate-treated rats. Moreover, treatment with Maca to Lead Acetate-treated rats resulted in lengths of stages VIII and IX–XI similar to the control group. Maca administration also reduced the deleterious effect on DSP caused by Lead Acetate treatment. Maca prevented LA-induced spermatogenic disruption in rats and it may become in a potential treatment of male infertility associated with Lead exposure.

D. Parent-massin - One of the best experts on this subject based on the ideXlab platform.

  • In vitro effect of Lead Acetate on human erythropoietic progenitors
    Cell Biology and Toxicology, 2001
    Co-Authors: R. Froquet, D. Parent-massin
    Abstract:

    Lead is known to induce hematological disturbances resulting from abnormalities in cell differentiation and hemoglobin synthesis during hematopoiesis. The aim of the present work was to study human erythropoiesis in vitro in the presence of Lead. Human erythroblastic progenitors, burst-forming units–erythroid (BFU-E), were exposed to Lead Acetate at increasing concentrations during 14 days of culture. Hematotoxicity was evaluated in vitro according to proliferation and differentiation of cell colonies arising from BFU-E development. The ability of cells to synthesize proteins, porphyrins, and hemoglobin was measured by spectrophotometric tests and by high-pressure liquid chromatography (HPLC). Results showed that in the presence of 10^–3 mol/L Lead Acetate, no hemoglobinized cells were observed in culture and no fluorescent porphyrins were detected in cells. Up to 10^–3 mol/L, Lead Acetate is not cytotoxic, i.e., it does not induce cell destruction. The present work demonstrates that Lead Acetate interferes with the porphyrin synthesis of human erythroblastic progenitors in vitro . The decrease of porphyrin content with 10^–5 mol/L Lead Acetate suggest that δ-aminolevulinic acid dehydratase can be inhibited by Lead Acetate during in vitro erythropoiesis . In vivo erythropoiesis occurs in the bone marrow. As about 95% of the body burden of Lead in adults is located in the bones with a biological half-life of some years, the concentration of Lead Acetate found to block porphyrin synthesis in vitro has to be compared with in situ bone marrow Lead concentrations.

  • In vitro effect of Lead Acetate on human erythropoietic progenitors.
    Cell Biology and Toxicology, 2001
    Co-Authors: B Rio, R. Froquet, D. Parent-massin
    Abstract:

    Lead is known to induce hematological disturbances resulting from abnormalities in cell differentiation and hemoglobin synthesis during hematopoiesis. The aim of the present work was to study human erythropoiesis in vitro in the presence of Lead. Human erythroblastic progenitors, burst-forming units-erythroid (BFU-E), were exposed to Lead Acetate at increasing concentrations during 14 days of culture. Hematotoxicity was evaluated in vitro according to proliferation and differentiation of cell colonies arising from BFU-E development. The ability of cells to synthesize proteins, porphyrins, and hemoglobin was measured by spectrophotometric tests and by high-pressure liquid chromatography (HPLC). Results showed that in the presence of 10(-3) mol/L Lead Acetate, no hemoglobinized cells were observed in culture and no fluorescent porphyrins were detected in cells. Up to 10(-3) mol/L, Lead Acetate is not cytotoxic, i.e., it does not induce cell destruction. The present work demonstrates that Lead Acetate interferes with the porphyrin synthesis of human erythroblastic progenitors in vitro. The decrease of porphyrin content with 10(-5) mol/L Lead Acetate suggest that delta-aminolevulinic acid dehydratase can be inhibited by Lead Acetate during in vitro erythropoiesis. In vivo erythropoiesis occurs in the bone marrow. As about 95% of the body burden of Lead in adults is located in the bones with a biological half-life of some years, the concentration of Lead Acetate found to block porphyrin synthesis in vitro has to be compared with in situ bone marrow Lead concentrations.

Heba M Abdou - One of the best experts on this subject based on the ideXlab platform.

  • protective role of omega 3 polyunsaturated fatty acid against Lead Acetate induced toxicity in liver and kidney of female rats
    BioMed Research International, 2014
    Co-Authors: Heba M Abdou, Mohamed A Hassan
    Abstract:

    The present study was conducted to investigate the protective role of Omega-3 polyunsaturated fatty acids against Lead Acetate-induced toxicity in liver and kidney of female rats. Animals were divided into four equal groups; group 1 served as control while groups 2 and 3 were treated orally with Omega-3 fatty acids at doses of 125 and 260 mg/kg body weight, respectively, for 10 days. These groups were also injected with Lead Acetate (25 mg/kg body weight) during the last 5 days. Group 4 was treated only with Lead Acetate for 5 days and served as positive control group. Lead Acetate increased oxidative stress through an elevation in MDA associated with depletion in antioxidant enzymes activities in the tissues. Moreover, the elevation of serum enzymes activities (ALT, AST, ALP, and LDH) and the levels of urea and creatinine were estimated but total proteins were decreased. Also, Lead Acetate-treatment induced hyperlipidemia via increasing of lipid profiles associated with decline in HDL-c level. Significant changes of Hb, PCV, RBCs, PLT, and WBCs in group 4 were recorded. The biochemical alterations of Lead Acetate were confirmed by histopathological changes and DNA damage. The administration of Omega-3 provided significant protection against Lead Acetate toxicity.

  • protective role of flax lignans against Lead Acetate induced oxidative damage and hyperlipidemia in rats
    Food and Chemical Toxicology, 2009
    Co-Authors: A A Newairy, Heba M Abdou
    Abstract:

    The results showed that the Lead concentration was higher than Cr, Ni and Cd in roadside soil samples. Also, the present study was conducted to investigate the protective role of flax lignans against the effects of Lead Acetate on oxidative stress, antioxidant enzymes and lipid profile. Animals were divided into three groups; the first group was used as control. While, groups 2, and 3 were orally treated with 200 mg/L Lead Acetate in drinking water and the combination of Lead Acetate (200 mg/L) plus flax lignans (30 mg/100 g BW), respectively. Rats were administered their respective doses daily for 3 weeks. Results showed that Lead Acetate increased TBARS, and decreased the activities of GST, SOD, GR and CAT, and the contents of glutathione in liver extracts, compared to control. The present data indicated that total lipids, cholesterol, triglycerides and LDL-c were significantly increased by Lead Acetate treatment, while HDL-c levels were decreased in the serum and liver extracts. Animals treated with flax lignans in combination with Lead Acetate alleviated its toxic effects in the tested parameters. Also, the morph metric analysis of the dorsal aorta revealed that, the histological alterations induced after Lead Acetate treatments were markedly reduced.

Sandra Yucra - One of the best experts on this subject based on the ideXlab platform.

  • lepidium meyenii maca reversed the Lead Acetate induced damage on reproductive function in male rats
    Food and Chemical Toxicology, 2006
    Co-Authors: Julio Rubio, Marissa I Riqueros, Manuel Gasco, Sandra Yucra, Sara Miranda, Gustavo F Gonzales
    Abstract:

    Abstract Rats were treated with 0, 8, 16 and 24 mg/kg of Lead Acetate (LA) (i.p.) for 35 days with or without Maca. Maca was co-administrated orally from day 18 to day 35. The lengths of stages of the seminiferous epithelium were assessed by transillumination. Also, sex organ weights, testicular and epididymal sperm count, sperm motility, daily sperm production, sperm transit rate and serum testosterone levels were measured. Lead Acetate treatment resulted in a dose–response reduction of lengths of stages VIII and IX–XI, and serum testosterone levels. However, rats treated with 8 and 16 mg/kg but not 24 mg/kg of Lead Acetate showed a low number of testicular spermatids, low daily sperm production (DSP) and low epididymal sperm count. Administration of Maca to rats treated with Lead Acetate resulted in higher lengths of stages VIII and IX–XI with respect to Lead Acetate-treated rats. Moreover, treatment with Maca to Lead Acetate-treated rats resulted in lengths of stages VIII and IX–XI similar to the control group. Maca administration also reduced the deleterious effect on DSP caused by Lead Acetate treatment. Maca prevented LA-induced spermatogenic disruption in rats and it may become in a potential treatment of male infertility associated with Lead exposure.