Antioxidant Defense, Oxidative Modification, and Salivary Gland Function in an Early Phase of Cerulein Pancreatitis

Abstract

Acute pancreatitis (AP) is a multifactorial disease characterized by necroinflammatory changes of the pancreas. Our study is the first study which evaluated the relationship between the free radical production, enzymatic and nonenzymatic antioxidants, oxidative damage, and secretory function of the salivary glands of AP rats. Male Wistar rats were divided equally into 2 groups: control (n=9) and AP (n=9). AP was induced by intraperitoneal injection with cerulein and confirmed by higher serum amylase and lipase. We have demonstrated that the superoxide dismutase and glutathione reductase activities, as well as reduced glutathione concentration, were significantly decreased in both the parotid and submandibular glands of AP rats as compared to the control rats. The production of free radicals evidenced as dichlorodihydrofluorescein assay and the activity of NADPH oxidase and xanthine oxidase and IL-1β concentration were significantly higher in the parotid and submandibular glands of AP rats compared to the controls. In AP rats, we also showed a statistical increase in oxidation modification products (advanced glycation end products and advanced oxidation protein products), salivary amylase activity, and significant decrease in the total protein content. However, we did not show apoptosis and any morphological changes in the histological examination of the salivary glands of AP rats. To sum up, cerulein-induced AP intensifies production of oxygen free radicals, impairs the redox balance of the salivary glands, and is responsible for higher oxidative damage to these glands. Interestingly, oxidative modification of proteins and dysfunction of the antioxidant barrier are more pronounced in the submandibular glands of AP rats.

Salivary Oxidative Stress Increases with the Progression of Chronic Heart Failure

“…A negative correlation between NWS salivary flow and AGE and MDA content, as well as a positive correlation between ROS production rate in SWS and AOPP concentration in HF patients may suggest the effect of oxidative stress on salivary gland dysfunction. It can be assumed that protein/lipid oxidation products are aggregated and accumulated in salivary glands, which-on the basis of positive feedback-boosts ROS production and leads to further oxidation of biomolecules [16,25,66]. In the end, the secretory cells of salivary glands are damaged, which is manifested by decreased production of NWS and SWS as well as disturbances in protein synthesis/secretion to saliva.…”

A Case-Control Study of Salivary Redox Homeostasis in Hypertensive Children. Can Salivary Uric Acid be a Marker of Hypertension?

“…Unfortunately, our study does not explain the causal relationship between oxidative stress and hyposalivation. However, it can be assumed that, as in other oxidative-stress-related diseases, products of protein and lipid oxidation can accumulate/aggregate in salivary glands, leading to secretory cell damage and a decrease in SWS secretion [21,22,49,68]. Indeed, oxidative stress is a key pathological factor responsible for hyposalivation in the course of many systemic diseases.…”

“…Similarly, the secretory function of salivary glands in hypertensive children has not been assessed so far. It is highly probable that, as in other oxidative stress-related diseases, the function of salivary glands as well as protein secretion in saliva are disturbed [21][22][23]. Because redox homeostasis cannot be characterized by a single biomarker, the aim of our study was to evaluate the salivary antioxidative barrier, the oxidative and nitrosative damage to proteins and lipids, as well as the secretory activity of salivary glands in children with hypertension compared to the controls.…”

A Longitudinal Study of the Antioxidant Barrier and Oxidative Stress in Morbidly Obese Patients after Bariatric Surgery. Does the Metabolic Syndrome Affect the Redox Homeostasis of Obese People?

“…The content of plasma advanced glycation end products (AGE) was assessed spectrofluorimetrically by measuring AGE-specific fluorescence at 350/440 nm [28]. Immediately before the assay, plasma samples were diluted (1:5, v:v) in 0.02 M phosphate-buffered saline (PBS), pH 7.4 [29]. The concentration of plasma advanced oxidation protein products (AOPP) was assessed spectrophotometrically at 340 nm by measuring the iodide ion oxidizing capacity of the plasma [28].…”

“…The concentration of plasma advanced oxidation protein products (AOPP) was assessed spectrophotometrically at 340 nm by measuring the iodide ion oxidizing capacity of the plasma [28]. Immediately before the assay, plasma was diluted (1:5, v:v) in 0.02 M PBS [29]. The concentration of plasma 4-hydroxynoneal protein adducts (4-HNE) and 8-isoprostanes (8-isop) was evaluated using commercial ELISA kits (OxiSelect HNE Adducts Competitive ELISA Kit, Cell Biolabs, Inc., San Diego, CA; 8-Isoprostane ELISA Kit, Cayman Chemicals, Ann Arbor, MI, USA; respectively), according to the manufacturer's instructions.…”