Salivary Redox Biomarkers in Different Stages of Dementia Severity.

This study is the first to evaluate oxidative stress biomarkers in saliva/blood of patients with varying degrees of dementia progression. The study included 50 healthy controls and 50 dementia patients divided into two groups: those with mild and moderate dementia (MMSE 11-23) and patients suffering from severe dementia (MMSE 0-10). Cognitive functions of the subjects were assessed using the Mini Mental State Examination (MMSE). Enzymatic and non-enzymatic antioxidants, oxidative damage products and protein glycoxidative modifications were determined in non-stimulated (NWS) and stimulated (SWS) saliva as well as erythrocyte/plasma samples. Generally, in dementia patients, we observed the depletion of antioxidant defences leading to oxidative and glycoxidative damage in NWS, SWS and blood samples. Both salivary and blood oxidative stress increased with the severity of the disease, and correlated with a decrease of cognitive functions. Interestingly, in dementia patients, reduced glutathione (GSH) in NWS correlated not only with the severity of dementia, but also with GSH concentration in the plasma. In receiver operating characteristic (ROC) analysis, we have demonstrated that salivary GSH clearly distinguishes patients with severe dementia from those suffering from mild or moderate dementia (area under the curve (AUC) = 1). Therefore, salivary GSH can be used as a non-invasive biomarker of cognitive impairment.

Antioxidant Defence, Oxidative Stress and Oxidative Damage in Saliva, Plasma and Erythrocytes of Dementia Patients. Can Salivary AGE be a Marker of Dementia?

Oxidative stress plays a crucial role in dementia pathogenesis; however, its impact on salivary secretion and salivary qualities is still unknown. This study included 80 patients with moderate dementia and 80 healthy age- and sex-matched individuals. Salivary flow, antioxidants (salivary peroxidase, catalase, superoxide dismutase, uric acid and total antioxidant capacity), and oxidative damage products (advanced oxidation protein products, advanced glycation end products (AGE), 8-isoprostanes, 8-hydroxy-2'-deoxyguanosine and total oxidant status) were estimated in non-stimulated and stimulated saliva, as well as in plasma and erythrocytes. We show that in dementia patients the concentration/activity of major salivary antioxidants changes, and the level of oxidative damage to DNA, proteins and lipids is increased compared to healthy controls. Non-stimulated and stimulated salivary secretions were significantly reduced in dementia patients. The deterioration in mini mental state examination (MMSE) score correlated with salivary AGE levels, which when considered with receiver operating characteristic (ROC) analysis, suggests their potential role in the non-invasive diagnosis of dementia. In conclusion, dementia is associated with disturbed salivary redox homeostasis and impaired secretory function of the salivary glands. Salivary AGE may be useful in the diagnosis of dementia.

Antioxidant profile, carbonyl and lipid oxidation markers in the parotid and submandibular glands of rats in different periods of streptozotocin induced diabetes.

OBJECTIVE: The aim of this study was to estimate the antioxidants barrier, and the oxidative stress in the salivary glands of rats in different periods of streptozotocin induced diabetes. DESIGN: Rats were divided in: 4 control (C2/4/10/14) and 4 experimental (DM2/4/10/14) groups. Salivary glands were removed 2/4/10/14 weeks after streptozotocin injection. Peroxidase (Px), uric acid (UA), total antioxidant status (TAS), superoxide dismutases (SODs), catalase (CAT), malonylodialdehyde (MDA), advanced glycation end products (AGE) concentrations were examined. RESULTS: TAS, Px were lower in the parotid diabetic glands throughout the whole experiment. TAS in the submandibular diabetic glands was lower in 2nd and 4th and higher in 14th week. Px in the submandibular diabetic glands was reduced in 4th and increased in 14th week. UA was lower in parotid, elevated in submandibular diabetic glands in 4th, 10th, 14th weeks. In the submandibular as compared to parotid glands an increase in TAS and UA was observed in 10th and 14th, Px in 14th week. In all periods, a significant increase in AGE was observed in both diabetic salivary glands. An increase in MDA was observed in the parotid diabetic glands in the 4th, 10th, 14th of the study. In the submandibular glands this increase was observed in the 2nd, 4th, 10th week, in the 14th week, the MDA level was significantly reduced in comparison to the control. CONCLUSION: The antioxidants of parotid glands are deficient throughout the whole experiment. In the last period submandibular glands copy with free radicals, becoming the main antioxidant's source.