Oxidative stress biomarkers in four Bloom syndrome (BS) patients and in their parents suggest in vivo redox abnormalities in BS phenotype

Adriana Zatterale, Frank J. Kelly, Paolo Degan, Marco d'Ischia, Federico V. Pallardó, Rita Calzone, Christina Dunster, Ana Lloret, Paola Manini, Ozgur Coǧulu, Kaan Kavakli, Giovanni Pagano

Research output: Contribution to journalArticle

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Abstract

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, α- and γ-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.

Original languageEnglish
Pages (from-to)1100-1103
Number of pages4
JournalClinical Biochemistry
Volume40
Issue number15
DOIs
Publication statusPublished - Oct 2007

Fingerprint

Bloom Syndrome
Oxidative stress
Biomarkers
Oxidation-Reduction
Oxidative Stress
Parents
Glutathione Disulfide
Phenotype
Plasmas
Glyoxal
Pyruvaldehyde
Tocopherols
Leukocytes
Uric Acid
Ascorbic Acid
Glutathione
Blood
Antioxidants
Association reactions
DNA

Keywords

  • 8-hydroxy-2′-deoxyguanosine
  • Ascorbic acid
  • Bloom syndrome
  • Glutathione
  • Glyoxal
  • Methylglyoxal
  • Oxidative stress
  • Uric acid

ASJC Scopus subject areas

  • Clinical Biochemistry

Cite this

Oxidative stress biomarkers in four Bloom syndrome (BS) patients and in their parents suggest in vivo redox abnormalities in BS phenotype. / Zatterale, Adriana; Kelly, Frank J.; Degan, Paolo; d'Ischia, Marco; Pallardó, Federico V.; Calzone, Rita; Dunster, Christina; Lloret, Ana; Manini, Paola; Coǧulu, Ozgur; Kavakli, Kaan; Pagano, Giovanni.

In: Clinical Biochemistry, Vol. 40, No. 15, 10.2007, p. 1100-1103.

Research output: Contribution to journalArticle

Zatterale, A, Kelly, FJ, Degan, P, d'Ischia, M, Pallardó, FV, Calzone, R, Dunster, C, Lloret, A, Manini, P, Coǧulu, O, Kavakli, K & Pagano, G 2007, 'Oxidative stress biomarkers in four Bloom syndrome (BS) patients and in their parents suggest in vivo redox abnormalities in BS phenotype', Clinical Biochemistry, vol. 40, no. 15, pp. 1100-1103. https://doi.org/10.1016/j.clinbiochem.2007.06.003
Zatterale, Adriana ; Kelly, Frank J. ; Degan, Paolo ; d'Ischia, Marco ; Pallardó, Federico V. ; Calzone, Rita ; Dunster, Christina ; Lloret, Ana ; Manini, Paola ; Coǧulu, Ozgur ; Kavakli, Kaan ; Pagano, Giovanni. / Oxidative stress biomarkers in four Bloom syndrome (BS) patients and in their parents suggest in vivo redox abnormalities in BS phenotype. In: Clinical Biochemistry. 2007 ; Vol. 40, No. 15. pp. 1100-1103.
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AU - Kelly, Frank J.

AU - Degan, Paolo

AU - d'Ischia, Marco

AU - Pallardó, Federico V.

AU - Calzone, Rita

AU - Dunster, Christina

AU - Lloret, Ana

AU - Manini, Paola

AU - Coǧulu, Ozgur

AU - Kavakli, Kaan

AU - Pagano, Giovanni

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N2 - 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, α- and γ-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.

AB - 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, α- and γ-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.

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