Protective effects of free radical scavengers and antioxidants against smokeless tobacco extract (STE)-induced oxidative stress in macrophage J774A.1 cell cultures

1995 ◽  
Vol 29 (3) ◽  
pp. 424-428 ◽  
Author(s):  
D. Bagchi ◽  
E.A. Hassoun ◽  
M. Bagchi ◽  
S.J. Stohs
Keyword(s):  
Oxidative Stress ◽  
Free Radical ◽  
Cell Cultures ◽  
Smokeless Tobacco ◽  
Free Radical Scavengers ◽  
Protective Effects ◽  
Radical Scavengers ◽  
Tobacco Extract

scholarly journals Molecular Mechanisms behind Free Radical Scavengers Function against Oxidative Stress

Antioxidants ◽  
2017 ◽  
Vol 6 (3) ◽  
pp. 51 ◽  
Author(s):  
Fereshteh Ahmadinejad ◽  
Simon Geir Møller ◽  
Morteza Hashemzadeh-Chaleshtori ◽  
Gholamreza Bidkhori ◽  
Mohammad-Saeid Jami
Keyword(s):  
Oxidative Stress ◽  
Free Radical ◽  
Molecular Mechanisms ◽  
Free Radical Scavengers ◽  
Radical Scavengers

Role of oxidative stress and heme oxygenase activity in morphine-induced glomerular epithelial cell growth

2003 ◽  
Vol 285 (5) ◽  
pp. F861-F869 ◽  
Author(s):  
Jaimita Patel ◽  
Nagarathna Manjappa ◽  
Rajani Bhat ◽  
Pavni Mehrotra ◽  
Madhu Bhaskaran ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Free Radical ◽  
Epithelial Cell ◽  
Heme Oxygenase ◽  
De Novo ◽  
Free Radical Scavengers ◽  
Opiate Addiction ◽  
Zinc Protoporphyrin ◽  
Radical Scavengers ◽  
Glomerular Epithelial Cell

Opiate addiction has been reported to contribute to the progression of renal injury. In addition, opiate addiction is a major risk factor for the development of human immunodeficiency virus-associated nephropathy. In the present study, we evaluated the effects of morphine, an active metabolite of heroin, on glomerular epithelial cell (GEC) growth and the involved molecular mechanism. At lower concentrations, morphine promoted GEC proliferation; however, at higher concentrations, morphine triggered apoptosis. Antioxidants inhibited morphine-induced proliferation as well as apoptosis. Similarly, free radical scavengers prevented morphine-induced GEC proliferation and apoptosis. Because proliferative and proapoptotic effects of morphine were inhibited by free radical scavengers as well as antioxidants, it appears that these effects of morphine are mediated through oxidative stress. Hemin, an inducer of heme oxygenase (HO) activity, inhibited GEC proliferation and promoted GEC apoptosis under basal and morphine-stimulated conditions. On the other hand, zinc protoporphyrin, an inhibitor of HO activity, promoted GEC proliferation and inhibited GEC apoptosis under basal as well as morphine-stimulated conditions. These findings suggest that HO activity is directly related to GEC apoptosis and inversely related to GEC proliferation. Morphine, de novo, had bimodal effects on HO activity: lower concentrations increased and higher concentrations decreased HO activity. It appears that HO activity may be modifying morphine-induced GEC growth.

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