Eur J Pediatr Surg 2021; 31(06): 541
DOI: 10.1055/s-0040-1713132
Letter to the Editor

Comment: Oxidative DNA Damage and NOX4 Levels in Children with Undescended Testes

1   Department of Pediatric Surgery, Faculty of Medicine, Gazi University, Ankara, Turkey
,
Zafer Turkyilmaz
1   Department of Pediatric Surgery, Faculty of Medicine, Gazi University, Ankara, Turkey
,
Kaan Sonmez
1   Department of Pediatric Surgery, Faculty of Medicine, Gazi University, Ankara, Turkey
› Author Affiliations
Funding None.

Oxidative DNA Damage and NOX4 Levels in Children with Undescended Testes

We read with great interest the article by Avci et al, “Oxidative DNA Damage and NOX4 Levels in Children with Undescended Testes.” This article has shown the serum levels of malondialdehyde (MDA), ischemia-modified albumin (IMA), nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4), and oxidative DNA damage (8-hydroxy 2 deoxyguanosine) in children with undescended testes (UDT) were significantly higher than that in the control group. In addition, they found that the levels of NOX4, IMA, and oxidative DNA damage after 12 months of age was significantly higher than that before 12 months of age. They state that “delay in the treatment of UDT may cause oxidative damage and antioxidant therapy may be beneficial in children with UDT.”[1]

In the study, the blood samples were obtained from patients with UDT aged 8 to 80 months and from healthy children aged of 7 to 88 months as controls. This is a very wide age range. If different groups were formed within the two groups with similar ages close to each other, it could be determined whether the oxidative stress increased with age or not. In addition, if different UDT localizations such as intra-abdominal and inguinal were included in the study, whether the oxidative stress changes with the localization of the testicle could also be determined. Also, if additional blood samples were obtained before 6 months of age, it could have been shown whether the oxidative stress increased before histological changes, making it possible to reveal a causal relationship for these changes. Lack of these determinations renders the hypothesis that UDT causes oxidative injury, resulting in histopathological changes specific to UDT obscure. We also believe that one of the most important limitations of this study is that oxidative parameter measurements were not determined following UDT treatment. The role of oxidative stress in tissue injury in UDT would be supported if this postoperative assessment was made and if oxidative values were normalized. If they were still high, the role of oxidative stress would be excluded for UDT, and despite the treatment of the UDT, the high values could indicate that the damage caused by the testicle with its altered histopathology to itself is still continuing. Similar publications in the literature did not support this issue with postoperative period values.[2] [3]

Due to lack of cases, budget, and time limitations, the aforementioned deficiencies may not have been covered; therefore, this issue should be addressed by further studies and samples of testicular tissue itself rather than only blood samples.



Publication History

Received: 23 March 2020

Accepted: 08 May 2020

Publication Date:
26 June 2020 (online)

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