Chlorhexidine induces DNA damage in rat peripheral leukocytes and oral mucosal cells

Objective: Chlorhexidine digluconate is widely used in dental practice for decreasing plaque control, controlling gingivitis and disinfecting root canals. However, the undesirable effects of chlorhexidine digluconate regarding its genotoxicity are conflicting in the literature. Thus, the aim of this study was to investigate the genotoxicity of chlorhexidine digluconate in rat peripheral blood and oral mucosal cells by the single cell gel (comet) assay and micronucleus assay.Methods: Thirty male Wistar rats were distributed into three groups: negative control; experimental group orally treated with 0.5 ml of 0.12% chlorhexidine digluconate, twice daily, during 8 days; and positive control, which received 4-nitroquinoline 1-oxide at 0.5 g/l by drinking water.Results: A statistically significant increase of DNA damage was observed in leukocytes and oral mucosal cells of the chlorhexidine digluconate treated group, as assessed by the comet assay. However, no increase of micronucleated cells was detected in reticulocytes from peripheral blood cells.Conclusions: Taken together, the data indicate that chlorhexidine digluconate is able to induce primary DNA damage in leukocytes and in oral mucosal cells, but no chromosome breakage or loss in erythrocytes.

Lack of genotoxicity induced by endogenous and synthetic female sex hormones in peripheral blood cells detected by alkaline Comet assay

The etiology of hormone-induced cancers has been considered to be a combination of genotoxic and epigenetic events. Currently, the Comet assay is widely used for detecting genotoxicity because it is relatively simple, sensitive, and capable of detecting various kinds of DNA damage. The present study evaluates the genotoxic potential of endogenous and synthetic sex hormones, as detected by the Comet assay. Blood cells were obtained from 12 nonsmoking and 12 smoking women with regular menstrual cycles and from 12 nonsmoking women taking low-dose oral contraceptives (OC). Peripheral blood samples were collected at three phases of the menstrual cycle (early follicular, mean follicular, and luteal phases), or at three different moments of oral contraceptive intake. Three blood samples were also collected from 12 healthy nonsmoking men, at the same time as oral contraceptive users. Results showed no significant difference in the level of DNA damage among the three moments of the menstrual cycle either in nonsmoking and smoking women, or between them. No significant difference in DNA damage was also observed among oral contraceptive users, nonusers, and men. Together, these data indicate lack of genotoxicity induced by the physiological level of the female sex hormones and OC as assessed by the alkaline Comet assay. In conclusion, normal fluctuation in endogenous sex hormones and use of low-doses of oral contraceptive should not interfere with Comet assay data when this technique is used for human biomonitoring.

Genotoxicity in primary human peripheral lymphocytes after exposure to radiopacifiers in vitro

Taking into consideration that DNA damage plays an important role in carcinogenesis, the purpose of this study was to evaluate whether some radiopacifiers widely used in clinical practice are able to induce genetic damage in primary human cells in vitro. Human peripheral lymphocytes obtained from 10 healthy volunteers were exposed to barium sulphate (BaSO(4)), zirconium oxide (ZnO(2)) and bismuth oxide (Bi(2)O(3)) at final concentrations ranging from 1 to 1000 mu g/mL for 1 h at 37 degrees C. The negative control group was treated with vehicle control (phosphate buffer solution) for 1 h at 37 degrees C and the positive control group was treated with hydrogen peroxide (at 100 mu M) for 5 min on ice. Results were analyzed by the Friedman non-parametric test. The results pointed all compounds tested out did not induce DNA breakage in human peripheral lymphocytes as depicted by the mean tail moment and tail intensity in all concentrations tested. In summary, our results indicate that exposure to these radiopacifiers may not be a factor that increases the level of DNA lesions in human peripheral lymphocytes as detected by single cell gel (comet) assay.

Peripheral Ossifying Fibroma

The peripheral ossifying fibroma (POF) is a common gingival growth usually arising from the interdental papilla. The anterior maxilla is the most common location of involvement. The etiology and pathogenesis of POF remains unknown. Some investigators consider it a neoplastic process, whereas others argue that it is a reactive process; in either case, the lesion is thought to arise from cells in the periodontal ligament. Trauma or local irritants, such as dental plaque, calculus, microorganisms, masticatory force, ill-fitting dentures, and poor quality restorations, have been implicated in the etiology of POF. The recommended treatment is the excisional biopsy; however, it can leave a defect if the procedure is not followed by a subepithelial connective tissue graft. The main objective of this article was to present a clinical case of excisional biopsy of a POF followed by a subepithelial connective tissue graft to correct the defect caused by the biopsy. The biopsy defect was satisfactorily repaired, and the lesion has not recurred after 6 years of follow-up.

Damage of the medial preoptic area impairs peripheral pilocarpine-induced salivary secretion

The existence of neural connections between the medial preoptic area (MPOA) and the salivary glands and the increase in salivation by thermal or electrical stimulation of the MPOA have suggested an important role of MPOA in the control of salivary gland function. Although direct cholinergic activation of the salivary glands induces salivation, recent studies have suggested that salivation produced by i.p. pilocarpine may also depend on the activation of central mechanisms. Therefore, in the present study, we investigated the effects of bilateral electrolytic lesions of the MPOA on the salivation induced by i.p. pilocarpine. Adult male Holtzman rats (n = 11-12/group) with bilateral sham or electrolytic lesions of the MPOA were used. One, five, and fifteen days after the brain surgery, under ketamine anesthesia, the salivation was induced by i.p. pilocarpine (1 mg/kg of body weight), and saliva was collected using preweighted small cotton balls inserted into the animal's mouth. Pilocarpine-induced salivation was reduced 1 and 5 days after MPOA lesion (341 +/- 41 and 310 +/- 35 mg/7 min, respectively, vs. sham lesions 428 +/- 32 and 495 +/- 36 mg/7 min, respectively), but it was fully recovered at the 15th day post-lesion (561 +/- 49 vs. sham lesion: 618 27 mg/7 min). Lesions of the MPOA did not affect baseline non-stimulated salivary secretion. The results confirm the importance of MPOA in the control of salivation and suggest that its integrity is necessary for the full sialogogue effect of pilocarpine. However, alternative mechanisms probably involving other central nuclei can replace MPOA function in chronically lesioned rats allowing the complete recovery of the effects of pilocarpine. (c) 2006 Published by Elsevier B.V.

Increased susceptibility to development of anhedonia in rats with chronic peripheral nerve injury: Involvement of sleep deprivation?

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

The effect of propolis on CCL5 and IFN-gamma expression by peripheral blood mononuclear cells from leishmaniasis patients

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Evaluation of chemopreventive activity of glutamine by the comet and the micronucleus assay in mice's peripheral blood

This research has evaluated the effects of enteral supplementation of glutamine in clastogens and genotoxic damages caused by the acute administration of cisplatin. For this. it was utilized Swiss mice distributed in eight experimental groups: control, cisplatin, glutamine, in three different doses and the combination of these with cisplatin. The results show that the glutamine was present in neither genotoxic nor mutagenic activity. When in association with glutamine and cisplatin, in simultaneous treatment, it was verified the frequency decreased of micronuclei and comets. The damage reduction percentages to the micronucleus ranged from 95.4 to 91.8% after 24 h of administration of these compounds and 76.7 to 56.8% after 48 h. In the same time the damage reduction percentages to the comet test ranged from 117.0 to 115.0%. The results suggest that glutamine is capable of preventing genotoxic and mutagenic damage according to the experimental design proposed. (C) 2009 Elsevier B.V. All rights reserved.