Oxidative stress underlies the pathomechanisms of toxic action of cadmium (Cd), including its damaging impact on the oral cavity. This study investigated whether the administration of an extract from Aronia melanocarpa L. berries (AME), characterized by their strong antioxidative potential, may have a beneficial impact on the oxidative-reductive status of the submandibular gland in an experimental model of low-level and moderate human environmental exposure to cadmium. The main markers of the antioxidative status (glutathione reductase, superoxide dismutase, catalase, reduced glutathione, total antioxidative status (TAS)), total oxidative status (TOS), oxidative stress index (OSI = TOS/TAS), and lipid peroxides, as well as cadmium concentration, were evaluated in the submandibular gland tissue of female Wistar rats who received a 0.1% aqueous AME and/or a diet containing 0, 1, and 5 mg Cd/kg for 3 and 10 months. The treatment with cadmium decreased the activities of antioxidative enzymes (29%–74%), reduced glutathione concentration (45%–52%), and TAS and increased TOS, resulting in the development of oxidative stress and enhanced concentration of lipid peroxides in the submandibular gland. The administration of AME at both levels of exposure to cadmium offered significant protection against these actions of this xenobiotic. After the 10 month exposure to the 1 and 5 mg Cd/kg diet, TAS was decreased by 77% and 83%, respectively, TOS, OSI, and lipid peroxides concentration were increased by 50% and 52%, respectively, 11.8-fold and 14.4-fold, respectively, and 2.3-fold and 4.3-fold, respectively, whereas, in the case of the extract co-administration, the values of these parameters did not differ compared to the control group. The results indicate that the consumption of aronia products under exposure to cadmium may have a beneficial impact on the oxidative-reductive status of the submandibular gland and prevent oxidative stress development and enhanced lipid peroxidation in this salivary gland.

Cadmium (Cd) is a strongly toxic heavy metal with prooxidative properties. Since the exposure of the general population to this metal is predicted to increase, effective methods are being sought to prevent its negative actions. One of them involves the use of the antioxidant potential of polyphenol compounds contained in black chokeberry fruit extract and their capability of complex formation with Cd2+. The study objective was to investigate whether the administration of A. melanocarpa fruit extract rich in polyphenol compounds during low and moderate exposures to cadmium can protect the parotid gland against oxidative damage. The study was conducted using the experimental model on female Wistar rats which were given 0.1% aqueous extract of Aronia melanocarpa fruit (AE) and/or cadmium at a concentration of 1 (Cd1) or 5 (Cd5) mg Cd/kg feed for 3 and 10 months, and on control animals. The exposure to Cd attenuated the enzymatic antioxidant barrier (catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx)) and increased the concentration of hydrogen peroxide (H2O2), protein carbonyl (PC) groups, and oxidized lipids (LPO) in parotid gland. These disorders led to a reduction in the total antioxidative status (TAS), an increase in the total oxidative state (TOS), and development of stress. The administration of AE at both levels of exposure to cadmium substantially improved the enzymatic antioxidant barrier (CAT, SOD, GPx) and prevented oxidative damage to cellular macromolecules (PC, LPO) and the increase in the level of H2O2, MPO, TOS, and stress indicator (OSI = TOS/TAS) in the parotid gland. Concluding, it should be stated that the consumption of aronia products may prevent oxidative/antioxidative imbalance induced by Cd and oxidative stress development in the parotid gland, thus protecting the gland from damage.

Cadmium is one of the main chemical pollutants found in the daily environment of developed countries. Cigarettes are a significant source of that metal, which makes it important in terms of oral cavity health. The aim of this study was to determine if increased supply of zinc in chronic exposure to cadmium might protect the sublingual gland structure against oxidative damage. The experiment took 12 months and was conducted on 72 adult male rats. They were randomized into 9 groups. Eight groups received cadmium in drinking water (as CdCl2) at 5 or 50 mg Cd/dm3 and/or zinc (as ZnCl2) at 30 or 60 mg Zn/dm3. The control group received regular water. In the sublingual gland of all animal groups, levels of oxidative parameters were measured. The oxidative stress index was calculated as a TOS/TAS ratio. Cadmium exposure at 5 mg and 50 mg Cd/dm3 induced oxidative stress in the sublingual glands of the rats. Cadmium reduced the TAS and GSH levels and increased LPO, H2O2, TOS, and OSI. In cadmium exposure conditions, increasing the supply of zinc by 79% or 151%, as compared to the standard dietary intake of this microelement, completely prevented the reduction of TAS and GSH levels and accumulation of LPO, H2O2, and TOS in the examined gland at both exposure levels to that metal. The outcome data confirm the protective effect of increased zinc intake on the sublingual gland tissue in chronic cadmium exposure.

Oxidative stress takes part in the pathomechanisms of many diseases, including oral disorders. The imbalance between oxidative and antioxidative processes may lead to periodontitis, osteitis, or oral cancers. Furthermore, many chemotherapeutics, e.g., metronidazole (MTZ), may also cause toxic reactions and affect oxidative reactions. The research focused on MTZ influence on oxidative destruction in the parotid and submandibular gland tissue in animal experimental model. Therefore, the concentrations of enzymatic and nonenzymatic markers of oxidative stress were measured in these two rat glands in the control and experimental MTZ-treated groups. The material for analysis included parotid and submandibular glands of male Wistar rats, which were treated with metronidazole for 7 days by gastric tube in a dose of 100 mg/kg b.w. On day 8, the material was obtained and frozen in temp. −80°C. Then, the following seven enzymatic and nonenzymatic parameters were measured: GPx, TOS, TAS, SOD, LPO, CAT, and GSH. The data were analysed using Statistica 10.0. Metronidazole treatment in the experimental model showed an increase in LPO, TOS, and TOS/TAS and a decrease in CAT, SOD, GPx, and TAS. The conclusions of this research were made. Metronidazole treatment in a dose of 100 mg/kg b.w. caused imbalance between oxidative and antioxidative reactions in the rat parotid and submandibular glands. An increase was observed in LPO, TOS, and TOS/TAS in both glands exposed to metronidazole. Decreased activity of CAT, SOD, GPx, and TAS was noted, which indicates attenuation of the gland antioxidative protective barrier.

Cadmium (Cd) is one of the most harmful xenobiotics to which humans are exposed, mainly by the oral route, throughout life. Preventive strategies are searched as low intoxication with this element, among others due to its prooxidative properties, can be deleterious to health and the exposure to it is continuously increasing. Recently, interest has been paid to plant raw materials with a high antioxidative potential to oppose the prooxidative properties of cadmium, such as black chokeberry (Aronia melanocarpa L. fruit), which is rich in polyphenolic compounds. The study was aimed at assessing whether the chokeberry extract may counteract the prooxidative impact of low-level and moderate repeated intoxication with cadmium on the sublingual salivary gland. The investigation was performed on 96 Wistar rats (females), which were treated with a 0.1% aqueous extract from chokeberries or/and a diet containing 1 or 5 mg Cd/kg for 3 and 10 months, and control animals. The intoxication with cadmium, in a dose- and time-dependent manner, attenuated the enzymatic and nonenzymatic antioxidative potential and increased the concentration of hydrogen peroxide and total oxidative status of the sublingual salivary gland resulting in an occurrence of oxidative stress, enhancement of lipid peroxidation, and oxidative injuries of proteins in this salivary gland. The treatment with the black chokeberry extract during the intoxication with cadmium prevented this xenobiotic-caused oxidative/reductive imbalance and oxidative modifications of proteins and lipids in the salivary gland. The above results allow the conclusion that the consumption of black chokeberry products during intoxication with cadmium can prevent oxidative stress and its consequences in the sublingual salivary gland and thus counteract the unfavourable impact of this xenobiotic on the oral cavity.