OBJECTIVE: To evaluate an association of Bloom syndrome (BS) phenotype with an in vivo prooxidant state. METHODS: The following endpoints were measured in 4 BS patients, their 6 parents, and 78 controls: a) leukocyte and urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG); b) blood glutathione (GSSG and GSH), c) plasma levels of some plasma antioxidants (uric acid, UA, ascorbic acid, AA, alpha- and gamma-tocopherol), and of glyoxal (Glx) and methylglyoxal (MGlx). RESULTS: Leukocyte 8-OHdG levels were significantly increased in the 4 BS patients vs. 40 controls (p=0.04), while the urinary 8-OHdG levels were non-significantly increased in BS patients. Glutathione disulfide levels and GSSG/GSH ratio were significantly decreased in BS patients vs. 44 controls (p=0.02). The plasma levels of UA in BS patients were significantly increased vs. 24 controls (p=0.005). No significant alterations were found in the in the plasma levels of Glx, MGlx, AA, and tocopherol. No changes in the tested parameters were found in the BS heterozygotes. CONCLUSION: This report shows a significant increase in oxidative DNA damage in leukocytes and in plasma UA levels from 4 BS patients. Should these data be confirmed in more extensive BS patient groups, an involvement of oxidative stress in the clinical BS phenotype might be suggested.
OBJECTIVE: To evaluate an association of Bloom syndrome (BS) phenotype with an in vivo prooxidant state. METHODS: The following endpoints were measured in 4 BS patients, their 6 parents, and 78 controls: a) leukocyte and urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG); b) blood glutathione (GSSG and GSH), c) plasma levels of some plasma antioxidants (uric acid, UA, ascorbic acid, AA, alpha- and gamma-tocopherol), and of glyoxal (Glx) and methylglyoxal (MGlx). RESULTS: Leukocyte 8-OHdG levels were significantly increased in the 4 BS patients vs. 40 controls (p=0.04), while the urinary 8-OHdG levels were non-significantly increased in BS patients. Glutathione disulfide levels and GSSG/GSH ratio were significantly decreased in BS patients vs. 44 controls (p=0.02). The plasma levels of UA in BS patients were significantly increased vs. 24 controls (p=0.005). No significant alterations were found in the in the plasma levels of Glx, MGlx, AA, and tocopherol. No changes in the tested parameters were found in the BS heterozygotes. CONCLUSION: This report shows a significant increase in oxidative DNA damage in leukocytes and in plasma UA levels from 4 BS patients. Should these data be confirmed in more extensive BS patient groups, an involvement of oxidative stress in the clinical BS phenotype might be suggested.
Authors: Jaimin Patel; Beverly A Baptiste; Edward Kim; Mansoor Hussain; Deborah L Croteau; Vilhelm A Bohr Journal: Carcinogenesis Date: 2020-12-31 Impact factor: 4.944
Authors: Giovanni Pagano; Annarita Aiello Talamanca; Giuseppe Castello; Mario D Cordero; Marco d'Ischia; Maria Nicola Gadaleta; Federico V Pallardó; Sandra Petrović; Luca Tiano; Adriana Zatterale Journal: Oxid Med Cell Longev Date: 2014-05-04 Impact factor: 6.543