RESUMO
OBJECTIVE: To investigate the use of systemic N-acetylcysteine and vitamin A in the prevention of gentamicin ototoxicity in rats. METHODS: Forty-two Wistar rats were divided into four groups according to treatment: intratympanic saline, intratympanic gentamicin, intraperitoneal vitamin A after intratympanic gentamicin, and intraperitoneal N-acetylcysteine after intratympanic gentamicin. Signal-to-noise ratio and distortion product otoacoustic emissions were evaluated in all groups. RESULTS: N-acetylcysteine had a significant protective effect at 1.5, 2, 3, 4, 6 and 8 kHz, whilst vitamin A had a significant protective effect at 2, 3, 4 and 6 kHz, as determined by the distortion product otoacoustic emission measurements. According to the signal-to-noise measurements, N-acetylcysteine had a significant protective effect at 1.5, 2, 3, 4, 6 and 8 kHz, whilst vitamin A had a significant protective effect at 3, 6 and 8 kHz. CONCLUSION: Gentamicin-induced hearing loss in rats may be prevented by the concomitant use of vitamin A and N-acetylcysteine. Specifically, N-acetylcysteine appeared to have a more protective effect than vitamin A for a greater range of noise frequencies.
Assuntos
Acetilcisteína/farmacologia , Antibacterianos/toxicidade , Sequestradores de Radicais Livres/farmacologia , Gentamicinas/toxicidade , Perda Auditiva/prevenção & controle , Emissões Otoacústicas Espontâneas/efeitos dos fármacos , Vitamina A/farmacologia , Vitaminas/farmacologia , Animais , Audição/efeitos dos fármacos , Perda Auditiva/induzido quimicamente , Masculino , Ratos , Ratos Wistar , Razão Sinal-RuídoRESUMO
OBJECTIVE: Although many clinical investigations have found a relationship between hearing loss and diabetes mellitus, the pathophysiology of this effect remains controversial. To date, the mechanisms of hearing loss in diabetic patients have been explained in terms of microangiopathy, neuropathy and encephalopathy. However, many reports indicate that some diabetic complications are associated with oxidative stress related to the diabetes itself. In the present study, we hypothesised that oxidative stress may be a cause of hearing loss in diabetic patients. METHODS: The study group comprised non-insulin dependent diabetic patients with no signs of microangiopathy or peripheral neuropathy. The control group comprised sex-, age- and body weight matched, non-diabetic subjects. Auditory function was evaluated using pure tone audiometry and tympanometry. Subjects with normal hearing and sensorineural hearing loss were included in the study, whereas subjects with conductive hearing loss were excluded. Both the study group (n = 63) and the control group (n = 37) were divided into subgroups based on the presence and absence of hearing loss. Oxidative stress was evaluated by measuring serum indicators of protein oxidation and lipid peroxidation, serum levels of nitric oxide and various non-enzymatic antioxidants, and the activity of various enzymatic antioxidants. RESULTS: The non-insulin dependent diabetic patients had significantly higher serum levels of protein oxidation products, nitric oxide, enzymatic antioxidant activity (i.e. glutathione peroxidase and superoxide dismutase), compared with the control group (p < 0.05). When we compared the groups in relation to the presence of hearing loss, the nitric oxide level was significantly increased in the diabetic group with good hearing, compared with diabetic patients with hearing loss (p = 0.014). In the diabetic group, a clear, negative correlation was observed between serum levels of nitric oxide and vitamins C and E, and hearing impairment (r = -0.395, r = -0.318, r = -0.500, respectively). There was also a positive correlation between serum vitamin C concentrations and hearing levels in the control group (r = 0.417). CONCLUSION: These results suggest that oxidative stress may play an important role in hearing impairment in diabetic patients. In this process, increased protein oxidation appears to be more important than lipid peroxidation. Nitric oxide may have a protective effect on hearing, as may some nonenzymatic antioxidants such as vitamin C and E.
Assuntos
Deficiência de Ácido Ascórbico/metabolismo , Diabetes Mellitus Tipo 2/sangue , Perda Auditiva/sangue , Estresse Oxidativo/fisiologia , Deficiência de Vitamina A/metabolismo , Antioxidantes/metabolismo , Deficiência de Ácido Ascórbico/complicações , Diabetes Mellitus Tipo 2/complicações , Feminino , Perda Auditiva/etiologia , Humanos , Masculino , Pessoa de Meia-Idade , Óxido Nítrico/metabolismo , Valores de Referência , Deficiência de Vitamina A/complicaçõesRESUMO
BACKGROUND: Nasal polyposis is one of the most common inflammatory pathologies of the nasal cavity. The aetiopathogenetic mechanisms of nasal polyp formation are still unclear. OBJECTIVES: The aim of this study was to investigate the serum leptin levels in patients with nasal polyposis. DESIGN: A randomised, prospective study was performed of 28 adult patients with nasal polyposis and 22 control subjects of a similar age, sex and body mass index. RESULTS: Serum leptin levels were 12.10 +/- 9.39 ng/ml in the nasal polyposis patients and 6.17 +/- 7.68 ng/ml in the controls. A significant difference (p = 0.021) was observed in the mean serum leptin levels between nasal polyposis patients and controls. CONCLUSION: Serum leptin levels were found to be significantly higher in patients with nasal polyposis. Leptin, apart from its primary role in the regulation of body weight and energy expenditure, may have a role in the inflammatory response of nasal polyposis.
Assuntos
Leptina/sangue , Pólipos Nasais/sangue , Adulto , Biomarcadores/sangue , Índice de Massa Corporal , Estudos de Casos e Controles , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Estudos ProspectivosRESUMO
BACKGROUND AND OBJECTIVES: Chronic nonspecific pharyngitis is a chronic inflammation of the pharynx. It is found worldwide, and treatment is difficult. The underlying aetiopathogenesis is still controversial. The aim of this study was to investigate Helicobacter pylori seroprevalence in chronic nonspecific pharyngitis patients without other possible causative factors for chronic pharyngeal irritation and without H. pylori gastric mucosal infection. MATERIALS AND METHODS: Forty-one patients with symptoms of chronic nonspecific pharyngitis and 30 healthy control subjects were enrolled in this prospective, controlled, clinical study. In both study and control groups, selected patients were shown to have gastric mucosa uninfected by H. pylori, as demonstrated by the 14C-urea breath test. Comprehensive otorhinolaryngological examination did not elicit any factor contributing to the chronic pharyngeal complaint. Serum H. pylori immunoglobulin G antibody titres were assayed using serum enzyme-linked immunosorbent assay. The difference between the study and control groups was analysed by the chi-square test (the likelihood ratio was used). RESULTS: Thirty-two of the 41 patients (78 per cent) and 14 of the 30 control subjects (46.7 per cent) were found to be H. pylori positive. Patients with chronic nonspecific pharyngitis were found to have a significantly higher rate of H. pylori seropositivity than the control group (p = 0.016). CONCLUSION: These data may be important in developing future treatment strategies for chronic nonspecific pharyngitis.