Abstract
Background/objectivesPrevious studies have shown that N-acetylcysteine (NAC) supplementation with the simultaneous inclusion of HFD prevents salivary glands from oxidative stress and mitochondrial dysfunction. In this experiment, we examined if NAC supplementation could reverse the harmful effect of HFD on mitochondrial function, reduce the severity of apoptosis, and the activity of pro-oxidative enzymes in the salivary glands of rats with confirmed hyperglycemia.Subjects/methodsWistar rats were fed the standard or high-fat (HFD) diet for 10 weeks. After 6 weeks of the experiment, HFD rats were diagnosed with hyperglycemia and for the next 4 weeks, the animals were given NAC intragastrically. In the mitochondrial fraction of the parotid (PG) and submandibular salivary glands (SMG), we assessed redox status, inflammation, and apoptosis.ResultsThe inclusion of NAC increased the activity of mitochondrial complexes I and II + III as well as decreased the concentration of interleukin-1β, tumor necrosis factor α, and caspase-3, but only in the parotid glands of rats with hyperglycemia compared to the HFD group. However, N-acetylcysteine supplementation did not reduce the activity of caspase-9 or the Bax/Bcl-2 ratio in PG and SMG mitochondria. In both salivary glands we observed reduced activity of cytochrome c oxidase, NADPH oxidase, and xanthine oxidase, as well as hindered production of ROS and lower ADP/ATP radio, but the levels of these parameters were not comparable to the control group.ConclusionsWe demonstrated that NAC supplementation restores the glutathione ratio only in the mitochondria of the submandibular salivary glands. The supply of NAC did not significantly affect the other measured parameters. Our results indicate that NAC supplementation provides little protection against free radicals, apoptosis, and inflammation in the salivary gland mitochondria of HFD rats. Stimulated salivary secretion in hyperglycaemic rats supplemented with NAC seems to be closely related to mitochondrial respiratory capacity and appropriate ATP level.
Highlights
Chronic exposure to the high-fat diet (HFD) interferes with the body’s carbohydrate metabolism and contributes to the dysregulation of mitochondrial activity [1,2,3]
We examined if NAC supplementation could reverse the harmful effect of HFD on mitochondrial function, reduce the severity of apoptosis, and the activity of pro-oxidative enzymes in the salivary glands of rats with confirmed hyperglycemia
The activity of mitochondrial complexes II + III in the parotid glands of HFD rodents was significantly lower in comparison with the control group (↓24% p < 0.0001)
Summary
Chronic exposure to the high-fat diet (HFD) interferes with the body’s carbohydrate metabolism and contributes to the dysregulation of mitochondrial activity [1,2,3]. Our previous research found that HFD disrupts the function of the mitochondria, decreases ATP production, and enhances reactive oxygen species (ROS) formation in the salivary glands [2]. Hyperglycemia is accompanied by an increased rate of ADP regeneration, with reduced ATP production and increased depolarization of mitochondrial membranes [6]. NAC improves the activity of the mitochondrial complexes (I and IV) in the liver [9], completely restores the function of the complex II in the heart mitochondria and partially complex I in the mitochondria of the brain of aging rats [10]. The administration of NAC up to 2 h after the brain injury resulted in an improvement in the activity of mitochondrial complexes, enhanced oxidative phosphorylation, and a reduction in the rate of ROS production [11]. The Received: 3 April 2021 Revised: 20 September 2021 Accepted: 22 October 2021 restoration of mitochondrial function resulted from an increase in disulfide bonds of protein chains of the mitochondrial enzymes
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