Buprenorphine and Methadone as Opioid Maintenance Treatments for Heroin-Addicted Patients Induce Oxidative Stress in Blood

Christonikos Leventelis, Nikolaos Goutzourelas, Aikaterini Kortsinidou, Ypatios Spanidis, Georgia Toulia, Antzouletta Kampitsi, Christina Tsitsimpikou, Dimitrios Stagos, Aristidis S Veskoukis, Demetrios Kouretas, Christonikos Leventelis, Nikolaos Goutzourelas, Aikaterini Kortsinidou, Ypatios Spanidis, Georgia Toulia, Antzouletta Kampitsi, Christina Tsitsimpikou, Dimitrios Stagos, Aristidis S Veskoukis, Demetrios Kouretas

Abstract

Buprenorphine and methadone are two substances widely used in the substitution treatment of patients who are addicted to opioids. Although it is known that they partly act efficiently towards this direction, there is no evidence regarding their effects on the redox status of patients, a mechanism that could potentially improve their action. Therefore, the aim of the present investigation was to examine the impact of buprenorphine and methadone, which are administered as substitutes to heroin-dependent patients on specific redox biomarkers in the blood. From the results obtained, both the buprenorphine (n = 21) and the methadone (n = 21) groups exhibited oxidative stress and compromised antioxidant defence. This was evident by the decreased glutathione (GSH) concentration and catalase activity in erythrocytes and the increased concentrations of thiobarbituric acid reactive substances (TBARS) and protein carbonyls in the plasma, while there was no significant alteration of plasma total antioxidant capacity (TAC) compared to the healthy individuals (n = 29). Furthermore, methadone revealed more severe oxidant action compared to buprenorphine. Based on relevant studies, the tested substitutes mitigate the detrimental effects of heroin on patient redox status; still it appears that they need to be boosted. Therefore, concomitant antioxidant administration could potentially enhance their beneficial action, and most probably, buprenorphine that did not induce oxidative stress in such a severe mode as methadone, on the regulation of blood redox status.

Figures

Figure 1
Figure 1
GSH concentration and catalase activity in the control group (n = 29) and the OMT patients as a whole (n = 42). ∗∗,∗∗∗Significantly different compared to the control group (p < 0.05 and p < 0.001, respectively).
Figure 2
Figure 2
GSH concentration and catalase activity in the control (n = 29), the BMT (buprenorphine) (n = 21), and the MMT (methadone) (n = 21) groups. ∗,∗∗∗Significantly different compared to the control group (p < 0.05 and p < 0.001, respectively). #Significantly different compared to the buprenorphine group (p < 0.05).
Figure 3
Figure 3
Protein carbonyl and TBARS concentrations in the control group (n = 29) and the OMT patients as a whole (n = 42). ∗∗∗Significantly different compared to the control group (p < 0.001).
Figure 4
Figure 4
Protein carbonyl and TBARS concentrations in the control (n = 29), the BMT (buprenorphine) (n = 21), and the MMT (methadone) (n = 21) groups. ∗∗,∗∗∗Significantly different compared to the control group (p < 0.01 and p < 0.001, respectively).
Figure 5
Figure 5
TAC levels in the control group (n = 29) and the OMT patients as a whole (n = 42).
Figure 6
Figure 6
TAC levels in the control (n = 29), the BMT (buprenorphine), (n = 21) and the MMT (methadone) (n = 21) groups.

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Source: PubMed

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