Limits...
Water Spinach, Ipomoea aquatic (Convolvulaceae), Ameliorates Lead Toxicity by Inhibiting Oxidative Stress and Apoptosis.

Dewanjee S, Dua TK, Khanra R, Das S, Barma S, Joardar S, Bhattacharjee N, Zia-Ul-Haq M, Jaafar HZ - PLoS ONE (2015)

Bottom Line: The effects on the expressions of apoptotic signal proteins were estimated by western blotting.The extract may offer the protective effect via counteracting with Pb mediated oxidative stress and/or promoting the elimination of Pb by chelating.The presence of substantial quantities of flavonoids, phenolics and saponins would be responsible for the overall protective effect.

View Article: PubMed Central - PubMed

Affiliation: Advanced Pharmacognosy Research Laboratory, Department of Pharmaceutical Technology, Jadavpur University, Kolkata, 700032, India.

ABSTRACT

Background: Ipomoea aquatica (Convolvulaceae), an aquatic edible plant, is traditionally used against heavy metal toxicity in India. The current study intended to explore the protective role of edible (aqueous) extract of I. aquatica (AEIA) against experimentally induced Pb-intoxication.

Methods: The cytoprotective role of AEIA was measured on mouse hepatocytes by cell viability assay followed by Hoechst staining and flow cytometric assay. The effect on ROS production, lipid peroxidation, protein carbonylation, intracellular redox status were measured after incubating the hepatocytes with Pb-acetate (6.8 μM) along with AEIA (400 μg/ml). The effects on the expressions of apoptotic signal proteins were estimated by western blotting. The protective role of AEIA was measured by in vivo assay in mice. Haematological, serum biochemical, tissue redox status, Pb bioaccumulation and histological parameters were evaluated to estimate the protective role of AEIA (100 mg/kg) against Pb-acetate (5 mg/kg) intoxication.

Results: Pb-acetate treated hepatocytes showed a gradual reduction of cell viability dose-dependently with an IC50 value of 6.8 μM. Pb-acetate treated hepatocytes exhibited significantly enhanced levels (p < 0.01) of ROS production, lipid peroxidation, protein carbonylation with concomitant depletion (p < 0.01) of antioxidant enzymes and GSH. However, AEIA treatment could significantly restore the aforementioned parameters in murine hepatocytes near to normalcy. Besides, AEIA significantly reversed (p < 0.05-0.01) the alterations of transcription levels of apoptotic proteins viz. Bcl 2, Bad, Cyt C, Apaf-1, cleaved caspases [caspase 3, caspase 8 and caspase 9], Fas and Bid. In in vivo bioassay, Pb-acetate treatment caused significantly high intracellular Pb burden and oxidative pressure in the kidney, liver, heart, brain and testes in mice. In addition, the haematological and serum biochemical factors were changed significantly in Pb-acetate-treated animals. AEIA treatment restored significantly the evaluated-parameters to the near-normal position.

Conclusion: The extract may offer the protective effect via counteracting with Pb mediated oxidative stress and/or promoting the elimination of Pb by chelating. The presence of substantial quantities of flavonoids, phenolics and saponins would be responsible for the overall protective effect.

No MeSH data available.


Related in: MedlinePlus

Effect on ROS production, lipid peroxidation, protein carbonylation, co-enzyme Q9, co-enzyme Q10, CAT, SOD, GPx, GR, GST and GSH in the absence (Pb-acetate) and existence of AEIA (Pb-acetate +AEIA) in experimental mice.Values are denoted as mean ± SE (n = 6). $Values significantly differed (p < 0.05) from differed Pb-acetate control. # Values significantly differed (p < 0.01) from normal control. * Values significantly differed (p < 0.05) from differed Pb-acetate control. ** Values significantly differed (p < 0.01) from differed Pb-acetate control. SOD unit, “U” is defined as μ-moles inhibition of NBT-reduction/min while CAT unit “U” is defined as H2O2 consumed/minute.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4608788&req=5

pone.0139831.g006: Effect on ROS production, lipid peroxidation, protein carbonylation, co-enzyme Q9, co-enzyme Q10, CAT, SOD, GPx, GR, GST and GSH in the absence (Pb-acetate) and existence of AEIA (Pb-acetate +AEIA) in experimental mice.Values are denoted as mean ± SE (n = 6). $Values significantly differed (p < 0.05) from differed Pb-acetate control. # Values significantly differed (p < 0.01) from normal control. * Values significantly differed (p < 0.05) from differed Pb-acetate control. ** Values significantly differed (p < 0.01) from differed Pb-acetate control. SOD unit, “U” is defined as μ-moles inhibition of NBT-reduction/min while CAT unit “U” is defined as H2O2 consumed/minute.

Mentions: Pb-intoxication significantly enhanced (p < 0.01) intercellular ROS-generation, lipid peroxydation and protein-carbonylation in the hepatic, renal, cardiac, cerebral and testicular tissues (Fig 6). Data set is available in S5 Table. AEIA treatment, however, could significantly reduce the extent of ROS production (p < 0.01), lipid peroxydation (p < 0.05–0.01) and protein carbonylation (p < 0.05–0.01) in the aforementioned tissues. The results of various treatments on mitochondrial-ubiquinols (coenzymes Q9 & Q10) in liver, kidney, brain, heart, and testes have been estimated (Fig 6). Total co-enzyme Q9 and Q10 levels in the tissues were significantly (p < 0.01–0.05) decreased in Pb-acetated treated groups (group II). Treatment with AEIA significantly elevated Q9 levels in liver and kidney, heart, brain and testes (p < 0.05) as compared with toxic control group. On other hand, co-enzyme Q10 levels have been found to be significantly elevated in hepatic (p < 0.01), renal (p < 0.01), cardiac (p < 0.05), brain (p < 0.05) and testicular (p < 0.05) tissues following AEIA treatment. In search of protective role of AEIA against Pb-toxicity, the effects on tissue redox markers viz. antioxidant enzymes and reduced glutathione were estimated (Fig 6). Data set is available in S6 Table. Pb-acetate treatment significantly (p < 0.05–0.01) decreased the levels of tissue antioxidant enzymes namely CAT, SOD, GR, GST and GPx in the selected tissues of experimental mice. In search of effect on tissue GSH levels, Pb-acetate treatment decreased GSH levels significantly (p < 0.01) in the selected tissues of experimental mice. However, AEIA treatment could significantly (p < 0.05–0.01) revert the Pb-acetate mediated reduction of tissue redox markers near to normal status.


Water Spinach, Ipomoea aquatic (Convolvulaceae), Ameliorates Lead Toxicity by Inhibiting Oxidative Stress and Apoptosis.

Dewanjee S, Dua TK, Khanra R, Das S, Barma S, Joardar S, Bhattacharjee N, Zia-Ul-Haq M, Jaafar HZ - PLoS ONE (2015)

Effect on ROS production, lipid peroxidation, protein carbonylation, co-enzyme Q9, co-enzyme Q10, CAT, SOD, GPx, GR, GST and GSH in the absence (Pb-acetate) and existence of AEIA (Pb-acetate +AEIA) in experimental mice.Values are denoted as mean ± SE (n = 6). $Values significantly differed (p < 0.05) from differed Pb-acetate control. # Values significantly differed (p < 0.01) from normal control. * Values significantly differed (p < 0.05) from differed Pb-acetate control. ** Values significantly differed (p < 0.01) from differed Pb-acetate control. SOD unit, “U” is defined as μ-moles inhibition of NBT-reduction/min while CAT unit “U” is defined as H2O2 consumed/minute.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4608788&req=5

pone.0139831.g006: Effect on ROS production, lipid peroxidation, protein carbonylation, co-enzyme Q9, co-enzyme Q10, CAT, SOD, GPx, GR, GST and GSH in the absence (Pb-acetate) and existence of AEIA (Pb-acetate +AEIA) in experimental mice.Values are denoted as mean ± SE (n = 6). $Values significantly differed (p < 0.05) from differed Pb-acetate control. # Values significantly differed (p < 0.01) from normal control. * Values significantly differed (p < 0.05) from differed Pb-acetate control. ** Values significantly differed (p < 0.01) from differed Pb-acetate control. SOD unit, “U” is defined as μ-moles inhibition of NBT-reduction/min while CAT unit “U” is defined as H2O2 consumed/minute.
Mentions: Pb-intoxication significantly enhanced (p < 0.01) intercellular ROS-generation, lipid peroxydation and protein-carbonylation in the hepatic, renal, cardiac, cerebral and testicular tissues (Fig 6). Data set is available in S5 Table. AEIA treatment, however, could significantly reduce the extent of ROS production (p < 0.01), lipid peroxydation (p < 0.05–0.01) and protein carbonylation (p < 0.05–0.01) in the aforementioned tissues. The results of various treatments on mitochondrial-ubiquinols (coenzymes Q9 & Q10) in liver, kidney, brain, heart, and testes have been estimated (Fig 6). Total co-enzyme Q9 and Q10 levels in the tissues were significantly (p < 0.01–0.05) decreased in Pb-acetated treated groups (group II). Treatment with AEIA significantly elevated Q9 levels in liver and kidney, heart, brain and testes (p < 0.05) as compared with toxic control group. On other hand, co-enzyme Q10 levels have been found to be significantly elevated in hepatic (p < 0.01), renal (p < 0.01), cardiac (p < 0.05), brain (p < 0.05) and testicular (p < 0.05) tissues following AEIA treatment. In search of protective role of AEIA against Pb-toxicity, the effects on tissue redox markers viz. antioxidant enzymes and reduced glutathione were estimated (Fig 6). Data set is available in S6 Table. Pb-acetate treatment significantly (p < 0.05–0.01) decreased the levels of tissue antioxidant enzymes namely CAT, SOD, GR, GST and GPx in the selected tissues of experimental mice. In search of effect on tissue GSH levels, Pb-acetate treatment decreased GSH levels significantly (p < 0.01) in the selected tissues of experimental mice. However, AEIA treatment could significantly (p < 0.05–0.01) revert the Pb-acetate mediated reduction of tissue redox markers near to normal status.

Bottom Line: The effects on the expressions of apoptotic signal proteins were estimated by western blotting.The extract may offer the protective effect via counteracting with Pb mediated oxidative stress and/or promoting the elimination of Pb by chelating.The presence of substantial quantities of flavonoids, phenolics and saponins would be responsible for the overall protective effect.

View Article: PubMed Central - PubMed

Affiliation: Advanced Pharmacognosy Research Laboratory, Department of Pharmaceutical Technology, Jadavpur University, Kolkata, 700032, India.

ABSTRACT

Background: Ipomoea aquatica (Convolvulaceae), an aquatic edible plant, is traditionally used against heavy metal toxicity in India. The current study intended to explore the protective role of edible (aqueous) extract of I. aquatica (AEIA) against experimentally induced Pb-intoxication.

Methods: The cytoprotective role of AEIA was measured on mouse hepatocytes by cell viability assay followed by Hoechst staining and flow cytometric assay. The effect on ROS production, lipid peroxidation, protein carbonylation, intracellular redox status were measured after incubating the hepatocytes with Pb-acetate (6.8 μM) along with AEIA (400 μg/ml). The effects on the expressions of apoptotic signal proteins were estimated by western blotting. The protective role of AEIA was measured by in vivo assay in mice. Haematological, serum biochemical, tissue redox status, Pb bioaccumulation and histological parameters were evaluated to estimate the protective role of AEIA (100 mg/kg) against Pb-acetate (5 mg/kg) intoxication.

Results: Pb-acetate treated hepatocytes showed a gradual reduction of cell viability dose-dependently with an IC50 value of 6.8 μM. Pb-acetate treated hepatocytes exhibited significantly enhanced levels (p < 0.01) of ROS production, lipid peroxidation, protein carbonylation with concomitant depletion (p < 0.01) of antioxidant enzymes and GSH. However, AEIA treatment could significantly restore the aforementioned parameters in murine hepatocytes near to normalcy. Besides, AEIA significantly reversed (p < 0.05-0.01) the alterations of transcription levels of apoptotic proteins viz. Bcl 2, Bad, Cyt C, Apaf-1, cleaved caspases [caspase 3, caspase 8 and caspase 9], Fas and Bid. In in vivo bioassay, Pb-acetate treatment caused significantly high intracellular Pb burden and oxidative pressure in the kidney, liver, heart, brain and testes in mice. In addition, the haematological and serum biochemical factors were changed significantly in Pb-acetate-treated animals. AEIA treatment restored significantly the evaluated-parameters to the near-normal position.

Conclusion: The extract may offer the protective effect via counteracting with Pb mediated oxidative stress and/or promoting the elimination of Pb by chelating. The presence of substantial quantities of flavonoids, phenolics and saponins would be responsible for the overall protective effect.

No MeSH data available.


Related in: MedlinePlus