Volume 22, Issue 4 (9-2019)                   J Arak Uni Med Sci 2019, 22(4): 28-39 | Back to browse issues page


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Samimi F, Baazm M, Eftekhar E, Jalali Mashayekh F. Effect of Coenzyme Q10 Supplementation on Liver Total Oxidant/Antioxidant Status in Streptozotocin-induced Diabetic Rats. J Arak Uni Med Sci 2019; 22 (4) :28-39
URL: http://jams.arakmu.ac.ir/article-1-6045-en.html
1- Department of Biochemistry and Genetics, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran.
2- Department of Anatomy, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran.
3- Endocrinology and Metabolism Research Center, Hormozgan University of Medical Sciences, Bandar Abbas, Iran.
4- Department of Biochemistry and Genetics, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran.; Department of Laboratory Sciences, Faculty of Paramedicine, Arak University of Medical Sciences, Arak, Iran. , mashayekhi@arakmu.ac.ir
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1. Introduction
Diabetes mellitus is a metabolic disease characterized by elevated blood glucose levels and impaired metabolism of carbohydrates, proteins, and lipids [1]. In diabetes, elevated blood sugar increases the production of reactive oxygen species that results in oxidative stress. Research findings suggest that complications and problems of diabetes may be partly related to oxidative stress [2]. Cells contain a variety of enzymatic and non-enzymatic antioxidants. The activity of these antioxidant compounds reduces the harmful effects of free radicals and prevents their oxidative stress [3]. Coenzyme Q10 (CoQ10) is one of the essential endogenous cellular antioxidants that can neutralize all kinds of free radicals [4, 8]. Studies indicate a close relationship between decreased CoQ10 level and the incidence of diabetes. Therefore, one of the suggested strategies to reduce the complications of oxidative stress in diabetes is to use CoQ10 [6]. The purpose of the present study was to compare the effect of CoQ10 on Total Oxidative Capacity (TOC), Total Antioxidant Status (TAS), and Oxidative Stress Index (OSI).
2. Materials and Methods
In this experimental study, 30 male Wistar rats were used. The rats were randomly divided into 5 groups, including three healthy control groups (saline, sesame oil [as vehicle] and CoQ10-treated [10 mg/kg/d in sesame oil]) [7], diabetic group, and CoQ10-treated diabetic group (10 mg/kg/d in sesame oil for 42 days). Induction of diabetes in rats was done by intraperitoneal injection of Streptozotocin (STZ) at a dose of 55 mg/kg, and its confirmation was done by measuring blood glucose level 72 h and one wk after induction. The rats with fasting blood glucose levels above 250 mg /dL were considered as diabetic. At the end of the experiment, the rats were anesthetized by intraperitoneal injection of ketamine (60 mg/kg) and xylazine (20 mg/kg). Then, their blood was taken from their hearts, and their liver tissue was also removed. Serum glucose and Malondialdehyde (MDA) levels, thiol groups, TOS, and TAC, were measured in homogenized liver tissue [14-18].
3. Results
Comparison of MDA levels in the study groups showed that the level of this marker significantly increased in the diabetic control group compared to the healthy control group (P=0.001). Treatment with CoQ10 in diabetic rats resulted in a significant decrease in MDA concentration compared to the diabetic control group (P=0.022). Moreover, the mean concentration of thiol groups in the diabetic group significantly decreased compared to control groups (P=0.001). Treatment with CoQ10 in diabetic rats had increased the concentration of thiol groups compared to the diabetic group, but this increase was not statistically significant (P=0.25).
The diabetic group showed a significant decrease in TAC compared to healthy control groups (P=0.01). Treatment with CoQ10 in diabetic rats increased TAC, but this increase was not statistically significant (P=0.77). Comparison of TOS in the study groups showed that the level of this factor in the diabetic group was significantly higher compared to that in the healthy control groups (P=0.001). Treatment with CoQ10 in diabetic rats resulted in a significant decrease in TOS compared to the diabetic group (P=0.03). Regarding the mean OSI in study groups, the diabetic group showed a significant increase compared to healthy control groups (P=0.001). Treatment of diabetic rats with CoQ10 resulted in a significant decrease in OSI compared to the diabetic group (P=0.028).
4. Discussion
In diabetes, the metabolism of carbohydrates, proteins, and lipids is disrupted, and this condition eventually leads to increased oxidative stress [19]. Oxidative stress acts as a detrimental factor in exacerbating the pathological status of diabetes and liver tissue damage. CoQ10 is a fat-soluble vitamin-like compound and is found within membrane phospholipid bilayers and intracellular membranes [24]. It also prevents the oxidation of lipoproteins by reducing and regenerating vitamin E (α-tocopherol) [23]. Also, it can regenerate known antioxidants such as ascorbate, tocopherol, and glutathione by converting their oxidized form to reduced form. CoQ10 increases the ratio of reduced to oxidized glutathione in the liver and decreases the levels of reactive oxygen species increases the activity of mitochondrial electron transport chain complexes, and finally lowers the effects of oxidative stress [26, 27].
The results of the present study showed that the induction of diabetes in rats increased TOS level, decreased TAC level, and increased OSI value in their liver. Daily intake of 10 mg/kg CoQ10 in diabetic rats decreased TOS and MDA levels but increased TAC and decreased OSI. Therefore, CoQ10 supplementation can reduce diabetes complications by reducing lipid peroxidation and oxidative stress-induced diabetes.
Ethical Considerations
Compliance with ethical guidelines

This study obtained its ethical approval from the Research Ethics Committee of Arak University of Medical Sciences (Code: IR.ARAKMU.REC.1397.119). All ethical principles of working on laboratory animals were according to their guidelines. 
Funding
This study was extracted from a research proposal (No: 3134) and was funded by the Deputy for Research and Technology of Arak University of Medical Sciences.

Authors' contributions
All authors have met standard writing based on the guidelines of the International Committee of Medical Journal Publishers (ICMJE).
Conflicts of interest
The authors declare no conflict of interest.
Acknowledgements
The authors would like to thank the Deputy of Research and Technology of Arak University of Medical Sciences and its biochemistry laboratory experts.

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Type of Study: Original Atricle | Subject: Basic Sciences
Received: 2019/03/25 | Accepted: 2019/06/19

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