RESUMO
The present study evaluated the effect of sodium saccharin on mouse tracheal epithelium, in relation to its possible structural alterations. Mice of the C3H strain were fed with standard pellets supplemented with sodium saccharin for 180 days. At that time the mice were sacrificed and their trachea were processed for transmission electronic microscopy. We demonstrated that sodium saccharin produces alterations in cellular surface cilia, with cytoplasmic excrescences and ciliary malformations. These results suggest that sodium saccharin is not an innocuous sweetener and that it may cause structural alterations in epithelial tissues.
Assuntos
Sacarina/farmacologia , Traqueia/efeitos dos fármacos , Animais , Epitélio/efeitos dos fármacos , Masculino , CamundongosRESUMO
Sodium saccharin has found to be a tumoral promoter in the rat's bladder epithelium, property not demonstrated in humans. Nevertheless, at present there's no references on the possible alterations produced by sodium saccharin in the epithelium of the mice colon. In this work we describe the alterations produced by low doses of sodium saccharin in the epithelium of the mice colon. The changer produced by sodium saccharin consist in pleomorphic microvill with variations of form, length diameter and curvature and demonstrate by transmission electron microscopy.
Assuntos
Colo/efeitos dos fármacos , Mucosa Intestinal/efeitos dos fármacos , Sacarina/efeitos adversos , Edulcorantes/efeitos adversos , Animais , Colo/patologia , Feminino , Absorção Intestinal/efeitos dos fármacos , Mucosa Intestinal/patologia , Mucosa Intestinal/ultraestrutura , Neoplasias Intestinais/induzido quimicamente , Masculino , Camundongos , Microscopia Eletrônica , Microvilosidades , SódioRESUMO
The effect of sodium ursodeoxycholate (U) on short-circuit current (SCC), an index of basal and stimulated net ion transport across isolated skins of Bufo arenarum toads, was tested. U inhibited basal SCC when added to the epidermal side of the skins. The inhibitory effect was reversible after rinsing the preparation during 60 min. U also inhibited the natriferic response to oxytocin, db-cAMP and theophylline by 82%, 49% and 47%, respectively. Inhibition of SCC by exposure to U was reversed by the polyene antibiotic nystatin. In turn, SCC induced by nystatin in the amiloride-treated skin was insensitive to U and blocked by ouabain, a Na+, K(+)-ATPase inhibitor. These results strongly suggest that the effect of U is exerted at the apical membrane of sodium transporting cells, and rule out the existence of an additional site of inhibitory action of U.
Assuntos
Pele/efeitos dos fármacos , Ácido Ursodesoxicólico/toxicidade , Potenciais de Ação/efeitos dos fármacos , Amilorida/farmacologia , Animais , Transporte Biológico Ativo/efeitos dos fármacos , Bucladesina/farmacologia , Bufo arenarum , Interações Medicamentosas , Epiderme/efeitos dos fármacos , Epiderme/fisiologia , Feminino , Técnicas In Vitro , Masculino , Nistatina/farmacologia , Ouabaína/farmacologia , Ocitocina/farmacologia , Fenômenos Fisiológicos da Pele , Sódio/urina , Teofilina/farmacologiaRESUMO
The atrial natriuretic peptide cardionatrin I (cardionatrin I is ANF 99-126) was used in studies directed to assess its effects on osmotic water permeability (Posm) and short-circuit current (SCC) in isolated toad skin. Results showed that ANF 99-126 (10(-7) M) added to the dermal side of the skin had no effect on basal Posm or SCC. However, ANF 99-126 (3.3 x 10(-8) M) was able to produce a 50% reversible inhibition of the maximal Posm response to angiotensin II (AII) (3.2 x 10(-8) M). These effects were seen when the skins were preincubated with ANF 99-126 for 10 min or less before the addition of AII. Longer preincubation appeared to inactivate ANF 99-126 through proteolysis. ANF 99-126(10(-7) M) failed to inhibit the SCC response to AII (10(-5) M) in toad skin. These results are compatible with a modulatory function for ANF on several systems including those involved in the regulation of extracellular fluid volume.
Assuntos
Angiotensina II/farmacologia , Fator Natriurético Atrial/farmacologia , Fragmentos de Peptídeos/farmacologia , Fenômenos Fisiológicos da Pele , Animais , Bufo arenarum , Diuréticos/farmacologia , Epitélio/efeitos dos fármacos , Epitélio/fisiologia , Feminino , Peixes , Técnicas In Vitro , Masculino , Permeabilidade , Ratos , Pele/efeitos dos fármacosRESUMO
1. The effect of the alpha-2 adrenergic agonist clonidine on short-circuit current (SCC) across isolated skins of Bufo arenarum toads was investigated. 2. Clonidine inhibited basal SCC in a dose-dependent manner. 3. Blockade of the effect of clonidine on basal SCC by the selective alpha-2 antagonist yohimbine supports the hypothesis that the inhibitory effect is mediated by the stimulation of alpha-2 adrenergic receptors. 4. The fact that the inhibitory effect of clonidine is higher in skins with spontaneous positive SCC than in the negative ones, and that the alpha-2 agonist was unable to alter amiloride-induced negative SCC suggests that the inhibitory effect of clonidine may probably be mediated by inhibition of sodium transport.