Glutathione S-transferases of human lung: Characterization and evaluation of the protective role of the α-class isozymes against lipid peroxidation

1992 ◽  
Vol 299 (2) ◽  
pp. 232-241 ◽  
Author(s):  
Sharad S. Singhal ◽  
Manju Saxena ◽  
Hassan Ahmad ◽  
Sanjay Awasthi ◽  
Abida K. Haque ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Human Lung ◽  
Protective Role ◽  
Glutathione S Transferases

Protective role of Royal Jelly (honeybee) on genotoxicity and lipid peroxidation, induced by petroleum wastewater, inAllium cepaL. root tips

2009 ◽  
Vol 30 (11) ◽  
pp. 1205-1214 ◽  
Author(s):  
Zafer Türkmen ◽  
Kültiğin Çavuşoğlu ◽  
Kürşat Çavuşoğlu ◽  
Kürşad Yapar ◽  
Emine Yalçin
Keyword(s):  
Lipid Peroxidation ◽  
Royal Jelly ◽  
Protective Role ◽  
Root Tips

scholarly journals Association of Genetic Polymorphisms in GSTP1, GSTM1, and GSTT1 Genes with Vesicoureteral Reflux Susceptibility in the Children of Southeast Iran

2020 ◽  
Author(s):  
Sima SHAHROKHZADEH ◽  
Azam SOLEIMANI ◽  
Dor-Mohammad KORDI-TAMANDANI ◽  
Mohammad Hossein SANGTARASH ◽  
Omid NEJATI ◽  
...  
Keyword(s):  
Vesicoureteral Reflux ◽  
Genetic Risk ◽  
Protective Role ◽  
Common Type ◽  
Chain Reaction ◽  
Eastern Iran ◽  
Multifunctional Enzymes ◽  
Glutathione S Transferases ◽  
Polymerase Chain

Background: Vesicoureteral reflux (VUR) disease is the most common type of urinary tract anomalies in children. Genetic risk factors may be associated with the etiology of VUR. The role of the Glutathione S-transferases (GSTs) as multifunctional enzymes is cellular oxidative stress handling. This is the first study aimed at evaluating the relative risk of GSTP1, GSTM1, and GSTT1 polymorphisms in VUR susceptibility in children and provides new important insights into the genetics of affected children. Methods: The study was done in 2013 in Sistan and Baluchestan University, eastern Iran. Genotyping of three GSTP1, GSTM1, and GSTT1 genes were determined using the multiplex polymerase chain reaction assay in 216 reactions for 72 VUR children and 312 reactions for 104 healthy controls. Results: The presence of GSTT1 deletion was associated with high risk of VUR in children, whereas GSTP1 and GSTM1 genotypes did not show the same effect. Furthermore, the combination of GSTT1/GSTM1 and GSTT1/ GSTP1 genotypes showed a significant influence on lower risk of VUR in children. Conclusion: Deletion of GSTT1 functional gene is a genetic risk factor causing VUR in children. Interestingly, the combination of GSTM1 and GSTP1 null genotypes with GSTT1 has shown a protective role against risk of GSTT1 deletion.

Protective Role of Raphanus Sativus Root Extract on Paracetamol-Induced Hepatotoxicity in Albino Rats

2007 ◽  
Vol 77 (1) ◽  
pp. 41-45 ◽  
Author(s):  
Chaturvedi ◽  
George ◽  
Machacha
Keyword(s):  
Lipid Peroxidation ◽  
Raphanus Sativus ◽  
Thiobarbituric Acid ◽  
Protective Role ◽  
Albino Rats ◽  
Root Extract ◽  
Dependent Manner ◽  
Dose Dependent ◽  
Serum Glutamate

The methanol extract of Raphanus sativus root extract showed a protective effect on paracetamol-induced hepatotoxicity in a dose-dependent manner. Degree of lipid peroxidation caused by paracetamol was measured in terms of thiobarbituric acid reactive substances (TBARS) and protection was measured in reference to serum glutamate oxaloacetate transaminase (SGOT), serum glutamate aspartate transaminase (SGPT), and blood and hepatic levels of antioxidants like glutathione and catalase. Administration of extract along with paracetamol showed significant protection. Levels of TBARS were found to be low, activities of SGOT and SGPT were low, while hepatic glutathione levels were significantly higher in experimental rats that received the mixture of paracetamol and the extract as compared to rats that received paracetamol only. Activities of catalase were also high in all experimental groups. Thus this study indicates the involvement of Raphanus sativus root extract with antioxidants like glutathione and catalase in rendering protection against paracetamol-induced lipid peroxidation and hepatotoxicity.

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