Abstract
A high-sucrose diet (HSD) is widely known for its cariogenic effects and promotion of obesity, insulin resistance, type 2 diabetes, and cancer. However, the impact of the HSD diet on the salivary gland function as well as the level of salivary oxidative stress is still unknown and requires evaluation. Our study is the first to determine both redox balance and oxidative injury in the parotid and submandibular glands of rats fed the HSD diet compared to the control group. We have demonstrated that uric acid concentration and the activity of superoxide dismutase and peroxidase varied significantly in both the submandibular and parotid glands of HSD rats vs. the control group. However, enhanced oxidative damage to proteins, lipids, and DNA (increase in advanced glycation end products, advanced oxidation protein products, 4-hydroxynonenal, and 8-hydroxy-2’-deoxyguanosine) was observed only in the parotid glands of HSD rats. Moreover, the HSD diet also reduced the total protein content and amylase activity in both types of salivary glands and decreased the stimulated salivary flow rate. To sum up, an HSD diet reduces salivary gland function and disturbs the redox balance of the parotid as well as submandibular salivary glands. However, the parotid glands are more vulnerable to both antioxidant disturbances and oxidative damage.
Highlights
IntroductionFree sugars (glucose, fructose) and sucrose are the main substrates used for energy production, which facilitates a positive energy balance [1]
Free sugars and sucrose are the main substrates used for energy production, which facilitates a positive energy balance [1]
Energy intake, and the weight of submandibular glands were comparable between high-sucrose diet (HSD) rats and the control group (Table 1)
Summary
Free sugars (glucose, fructose) and sucrose are the main substrates used for energy production, which facilitates a positive energy balance [1]. The pathogenesis of the above disturbances is generally complex and diverse, it has been demonstrated that excess production of reactive oxygen species (ROS) in the course of chronic high-sucrose consumption may be one of the factors facilitating initiation and progression of these metabolic disorders [9]. In these conditions, insufficiency of the antioxidant systems to combat excessive ROS generation leads to oxidative stress (OS) and redox abnormalities. There are numerous reports on the increased oxidative damage to human or experimental animal plasma, liver, skeletal muscles [4,5,7,8], and heart [6] in the course of a high-sucrose diet
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