การเปลี่ยนแปลงระดับ 8-OHdG ในปัสสาวะ: ตัวบ่งชี้ความเสียหายของ DNA  ในผู้รับการบำบัดการติดสารแอมเฟตามีน

Kanyakorn  Kanniyom; Jarunee Suthumwong; Narisa  K. Bordeerat

Authors

Kanyakorn Kanniyom Graduate Program in Medical Technology, Faculty of Allied Health Sciences, Thammasat University, Rangsit Campus, Pathum Thani Province, Thailand
Jarunee Suthumwong Health Department, Bangkok, Thailand
Narisa K. Bordeerat Graduate Program in Medical Technology, Faculty of Allied Health Sciences, Thammasat University, Rangsit Campus, Pathum Thani Province, Thailand

Keywords:

8-Hydroxydeoxygaunosine (8-OHdG), Oxidative stress, DNA damage, Amphetamine

Abstract

Reactive oxygen species (ROS) are a major cause of DNA damage through oxidative reactions. Drug abuse is one of the factors that induces ROS production in the body. Notably, 8-hydroxy-2’deoxyguanosine (8-OHdG) has been identified as a key biomarker indicating oxidative stress-induced DNA damage. This study aimed to measure 8-OHdG levels, as an indicator of DNA damage, in urine samples from amphetamine users undergoing treatment. The study included 104 participants from Kao Mai Clinic, Bangkok, who had urinary methamphetamine levels exceeding 1,000 ng/mL. The results showed that the average 8-OHdG level before treatment was 3.10 ± 2.2 ng/mL, which significantly decreased to 1.57 ± 1.8 ng/mL after treatment (p < 0.001). A moderate correlation was observed between urinary amphetamine levels and 8-OHdG levels (r² = 0.543). The diagnostic performance of 8-OHdG as a biomarker for tracking DNA damage showed an area under the curve (AUC) of 0.88, with a cutoff value of 1.90 ng/mL, sensitivity of 86.0%, and specificity of 67.0%. In conclusion, amphetamine addiction treatment effectively reduces DNA damage, as reflected by the significant reduction in urinary 8-OHdG levels. Therefore, 8-OHdG can serve as a reliable biomarker for monitoring DNA damage and evaluating therapeutic interventions during amphetamine addiction treatment programs.

References

Rawson RA, Condon TP. Why do we need an addiction supplement focused on methamphetamine? Addiction. 2007;102:1–4.

Huang MC, Yang SY, Lin SK, Chen KY, Chen YY, Kuo CJ, Hung YN. Risk of cardiovascular diseases and stroke events in methamphetamine users: a 10-year follow-up study. J Clin Psychiatry. 2016;77:1396–1403.

McDonnell-Dowling K, Kelly JP. The role of oxidative stress in methamphetamine-induced toxicity and sources of variation in the design of animal studies. Curr Neuropharmacol. 2017;15:300–314.

Chang K-H, Chen C-M. The role of oxidative stress in Parkinson’s disease. Antioxidants. 2020;9:461-491.

Kasai H. Analysis of a form of oxidative DNA damage, 8-hydroxy-2!-deoxyguanosine, as a marker of cellular oxidative stress during carcinogenesis. Mutat Res. 1997;387:147–163.

Cooke MS, Evans MD, Dizdaroglu M, Lunec J. Oxidative DNA damage: mechanisms, mutation, and disease. Faseb J. 2003;17:1195–1214.

Klungland A, Rosewell I, Hollenbach S, Larsen E, Daly G, Epe B, Seeberg E, Lindahl T, Barnes DE. Accumulation of premutagenic DNA lesions in mice defective in removal of oxidative base damage. PNAS. 1999; 96: 13300 - 13305.

Cooke MS, Evans MD, Dove R, Rozalski R, Gackowski D, Siomek A, Lunec J, Olinski R. DNA repair is responsible for the presence of oxidatively damaged DNA lesions in urine. Mutat Res. 2005;574:58–66.

Kawai K, Kasai H, Li Y-S, Kawasaki Y, Watanabe S, Ohta M, et al. Measurement of 8-hydroxyguanine as an oxidative stress biomarker in saliva by HPLC-ECD. Genes and Environment. 2018;40:5.

Huang MC, Lai YC, Lin SK, Chen CH. Increased blood 8-hydroxy-2-deoxyguanosine levels in methamphetamine users during early abstinence. Am J Drug Alcohol Abuse. 2018;44(3):395-402.

Yamamoto BK, Raudensky J. The role of oxidative stress in methamphetamine-induced neurotoxicity and neuronal death. Neurotox Res. 2008;13:223–34.

Cadet JL, Brannock C, Krasnova IN. Molecular bases of methamphetamine-induced neurodegeneration. Int Rev Neurobiol. 2015;120:71–97.

Hagan CE, Sullivan KM, Liu SY. Oxidative stress and drug abuse: The role of free radicals in addiction. Neurosci Biobehav Rev. 2012;36:1130–40.

Monti PM, Rohsenow DJ, Hutchison KE. Toward bridging the gap between biological, psychobiological, and psychosocial models of alcohol craving. Addiction. 2000;95:S229–37.

Evans MD, Dizdaroglu M, Cooke MS. Oxidative DNA damage and disease: Induction, repair, and significance. Mutat Res. 2004;567:1–16.