Piotr Buczko

Oxidative Modification of Biomolecules in the Nonstimulated and Stimulated Saliva of Patients with Morbid Obesity Treated with Bariatric Surgery

Morbid obesity leads to progressive failure of many human organs and systems; however, the role of oxidative damage to salivary composition is still unknown in the obese patients. In this study, we assessed the effect of bariatric surgery on oxidative damage in nonstimulated (NS) and stimulated (S) whole saliva. The study included 47 subjects with morbid obesity as well as 47 age- and gender-matched healthy volunteers. Oxidative modifications to lipids (4-hydroxynonenal (4-HNE) and 8-isoprostanes (8-isoP)), proteins (advanced oxidation protein products (AOPP) and protein carbonyl groups (PC)), and DNA (8-hydroxy-D-guanosine (8-OHdG)) were analyzed in morbidly obese patients before and after bariatric surgery as well as in the healthy controls. The concentrations of 8-isoP, AOPP, PC, and 8-OHdG were significantly higher in both NS and S of patients with morbid obesity than in the control patients and compared to the results obtained 6 months after bariatric surgery. The levels of oxidative damage markers were also higher in S versus NS of morbidly obese patients. In summary, morbid obesity is associated with oxidative damage to salivary proteins, lipids, and DNA, while bariatric treatment generally lowers the levels of salivary oxidative damage.

Orthodontic treatment modifies the oxidant–antioxidant balance in saliva of clinically healthy subjects

PURPOSE The aim of our study was to analyse salivary markers of oxidative stress and an antioxidant response in clinically healthy subjects with fixed orthodontic appliances. MATERIAL/METHODS 37 volunteers were included in the study. Unstimulated (UWS) and stimulated (SWS) whole saliva were analysed for oxidative and antioxidant status and nickel levels immediately before the insertion of the appliances, an one week after and twenty four weeks after the insertion of fixed appliances. RESULTS A significant increase in tiobarbituric acid reactive substance (TBARS) and total oxidant status (TOS) one week, and total protein concentration twenty four weeks after the attachment of orthodontic appliances was found in the saliva. The markers of antioxidant status: superoxide dismutase (SOD), catalase (CAT), uric acid (UA), peroxidase (Px), and total antioxidant status (TAS) were not changed in all periods in UWS. In SWS a significant decrease in SOD1 and CAT was found whereas Px was increased one week after treatment and UA twenty four weeks following treatment. TAS was decreased in UWS and SWS twenty four weeks after orthodontic treatment. Oxidative status index (OSI) was elevated both in UWS and SWS one week after orthodontic treatment in comparison to the results obtained before and twenty four weeks. One week after treatment an increased concentration of nickel was also observed. CONCLUSIONS Orthodontic treatment modifies the oxidative-antioxidative balance in the saliva of clinically healthy subjects. Increased nickel concentration in saliva, released from orthodontic appliances, seems to be responsible for changes in the oxidative status of the saliva.

Caspase-3 as an important factor in the early cytotoxic effect of nickel on oral mucosa cells in patients treated orthodontically

INTRODUCTION The effect of fixed orthodontic appliances on biochemical changes in saliva and pathophysiological status of the oral cavity is not clear. Recent data showed that nickel (Ni) released from orthodontic appliances can decrease cellular viability, induce DNA damage and apoptosis in oral mucosa cells. Since the mechanism of these Ni effects is unknown, the aim of our study was to analyze the expression of caspase-3 in epithelial cells of oral mucosa in healthy individuals treated orthodontically. MATERIAL AND METHODS Twenty-eight volunteers participated in the study. Epithelial cells were collected from oral mucosa directly before appliance insertion, one week after the insertion, and 24 four weeks after the insertion of fixed appliances. Cellular identification and measurements were conducted by light microscopy. Caspase-3 expression was evaluated immunochemically. Nickel concentration in saliva was also determined. RESULTS A significantly higher number of oral epithelial cells with caspase-3 immunoreactivity in was found one week, but not 24 weeks, after orthodontic treatment. The enhanced expression of caspase-3 was accompanied by increased nickel concentration in saliva. CONCLUSIONS Our data suggests that nickel released from orthodontic appliances can activate caspase-3 and this mechanism may be partially responsible for the cytotoxic action of nickel in the oral cavity of orthodontically-treated individuals.

An important pathway of apoptotic effect of nickel early released from orthodontic appliances – Preliminary data

BACKGROUND Limited data demonstrate the effect of nickel released from orthodontic appliances. The mechanism of this action is not clear. The present study aimed to investigate the role of kynurenines, oxidative stress and caspase pathway in the mechanism of nickel action. METHODS We studied the concentration of nickel, 3-hydroxykynurenine, total oxidative status in saliva and caspase-3 in epithelial cells in 10 subjects before and one week after orthodontic treatment. RESULTS Orthodontic appliances significantly enhanced the concentration of nickel, 3-hydroxykynurenine, total oxidative status and augmented the expression of caspase-3 seven days after treatment in the oral cavity in respect to pre-treatment values. CONCLUSION Our data suggest that nickel released from orthodontic appliances activate tryptophan metabolism in oral cavity via the kynurenine pathway. The metal directly or through kynurenines enhancement activates oxidative stress and then via the caspase pathway induce apoptosis of buccal epithelial cells.