Lipid peroxidation in female dogs bearing mammary gland carcinomas

RESUMO O estresse oxidativo causa peroxidação lipídica e formação de substâncias reativas ao ácido tiobarbitúrico (TBARS), processo que está comprovadamente associado à progressão de neoplasias malignas em seres humanos. Por sua vez, espécies reativas de oxigênio (EROs) são produzidas no processo carcinogênico, de forma que a geração de EROs parece ser, ao mesmo tempo, causa e consequência dele. Em cães, a associação da peroxidação lipídica com a carcinogênese permanece ainda obscura, com estudos escassos, de resultados conflitantes, que, muitas vezes, incluem, dentro de um mesmo grupo amostral, animais portadores de tumores heterogêneos dos pontos de vista morfológico e comportamental, além de estes se apresentarem em estágios bastante distintos. Nesse contexto, buscou-se, na presente investigação, avaliar a concentração plasmática de TBARS em fêmeas hígidas e portadoras de carcinomas mamários com diagnóstico histopatológico de carcinoma mamário tubular simples estágio 4, com comprometimento de linfonodos, porém sem metástases detectadas. Foi observado que as cadelas diagnosticadas com carcinoma mamário tiveram níveis plasmáticos de TBARS significativamente maiores (média de 7,98 ± 1,43μmol/mL, p < 0,0001) em relação às fêmeas consideradas hígidas (média de 6,14 ± 0,53μmol/mL), o que sugere associação entre câncer e maior ocorrência de estresse oxidativo

Blood-brain Barrier Breakdown Following Gliotoxic Drug Injection In The Brainstem Of Wistar Rats [ruptura Da Barreira Hematoencefàlica Após Injeção De Droga Gliotóxica No Tronco Encefálico De Ratos Wistar]

Ethidium bromide (EB) causes local astrocytic disappearance, with glia limitans disruption and supposed blood-brain barrier (BBB) breakdown The aim of this study was to investigate the BBB integrity after the injection of 0.1% EB (group E) or 0.9% saline solution (group C) into cisterna pontis of Wistar rats. Brainstem fragments were collected from 24 hours to 31 days post-injection for ultrastructural study and GFAP immuno-histochemical staining. Some animals received colloidal carbon ink by intravenous route at the same periods. In rats from group C, there was no sign of astrocyte loss and no leakage of ink from blood vessels in the injection site. In group E, astrocyte disappearance began at 48 hours and some areas were still devoid of astrocytic processes 31 days after. Leakage of carbon particles was seen from 48 hours to 7 days in the EB-induced lesions. Tight junctions did not show any detectable ultrastructural change due to the lack of perivascular astrocytes.603 A582589Bondan, E.F., Lallo, M.A., Graça, D.L., Desmielinizaçao experimental por brometo de etídio no sistema nervoso central (1998) Rev Univ Guarulhos -Ciênc Biol Saúde, 5, pp. 19-32Bondan, E.F., Lallo, M.A., Graça, D.L., (1998) Efeitos do brometo de etídio no tronco encefálico de ratos Wistar imunossuprimidos com ciclosporina, pp. 1-46. , São Paulo: Coleção Cadernos de Estudos e Pesquisas UNIPBondan, E.F., Graça, D.L., Sinhorini, I.L., Lallo, M.A., Silva, I.M., Pharmacological interference on remyelination in rats submitted to the ethidium bromide model (1998) Arch Anat Cytol Path/Clin Exp Path, 46, p. 536Bondan, E.F., Lallo, M.A., Sinhorini, I.L., Graça, D.L., Schwann cells may express an oligodendrocyte-like remyelinating pattern following ethidium bromide injection in the rat brainstem (1999) Acta Microscopica, 8, pp. 707-708Bondan, E.F., Lallo, M.A., Sinhorini, I.L., Baz, E.I., Paulino, C.A., Graça, D.L., Ultrastructural investigation on the brainstem remyelination after local ethidium bromide injection in rats immunosuppressed with dexamethasone (1999) Acta Microscopica, 8, pp. 709-710Bondan, E.F., Lallo, M.A., Sinhorini, I.L., Pereira, L.A.V., Graça, D.L., The effect of cyclophosphamide on brainstem remyelination following ethidium bromide injection in Wistar rats (2000) J Submicrosc Cytol Pathol, 32, pp. 603-612Graça, D.L., (1986) Investigation into ethidium bromide induced-demyelination in the central nervous system, , Thesis (PhD), University of Cambridge, CambridgeGraça, D.L., Blakemore, W.F., Delayed remyelination in rat spinal cord following ethidium bromide injection (1986) Neuropathol Appl Neurobiol, 12, pp. 593-605Graça, D.L., Pereira, L.A.V., (1990) Dinâmica da impregnaça̧o celular pelo brometo de etídio "in vitro" e "in vivo" (Abstr), pp. 430-431. , Porto Alegre: Anais da 42a Reunia̧o da Sociedade Brasileira para o Progresso da Ciência (SBPC)Pereira, L.A.V., Dertkigill, M.S.J., Graça, D.L., Cruz-Höfling, M.A., Dynamics of remyelination in the brain of adult rats after exposure to ethidium bromide (1998) J Submicrosc Cytol Pathol, 30, pp. 341-348Yajima, K., Suzuki, K., Ultrastructural changes of oligodendroglia and myelin sheats induced by ethidium bromide (1979) Neuropathol Appl Neurobiol, 5, pp. 49-62Yajima, K., Suzuki, K., Demyelination and remyelination in the rat central nervous system following ethidium bromide injection (1979) Lab Invest, 41, pp. 385-392Bondan, E.F., Lallo, M.A., Mielinizaça̧o, desmielinizaça̧o e remielinizaça̧o no SNC: Aspectos histofisiológicos relevantes à formaça̧o e integridade da mielina central (1998) Rev Inst Ciênc Saúde, 16, pp. 103-111Leibowitz, S., Hughes, R.A.C., (1983) Immunology of the nervous system, pp. 2-16. , London: Edward ArnoldSternberger, N.H., Multiple sclerosis as a autoimunne disease: Vascular antigens (1989) Res Immunol, 140, pp. 181-187Janzer, R.C., Raff, M.C., Astrocytes induce blood-brain barrier properties in endothelial cells (1987) Nature, 325, pp. 253-257Risau, W., Induction of blood-brain barrier endothelial cell differentiation (1991) Ann NY Acad Sci, 405, pp. 405-419Peters, A., Palay, S.L., Webster HdeF, (1991) The fine structure of the nervous system. 3. Ed., pp. 290-295. , New York: Oxford Univ PressStewart, P.A., Coomber, B.L., Astrocytes and the blood-brain barrier (1986) Astrocytes: development, morphology and regional specializations of astrocytes, pp. 311-323. , Fedoroff S, Verdanakis A (eds.). London: Academic PressBundgaard, M., Pathways across the vertebrate blood-brain barrier: Morphological viewpoints (1986) Ann NY Acad Sci, 481, pp. 7-18Reese, T.S., Karnovsky, M.J., Fine structural localization of a blood-brain barrier to exogenous peroxidase (1967) J Cell Biol, 34, pp. 207-217Felts, P.A., Smith, K.J., Tilt, E., Blood-brain barrier function in central demyelinating lesions repaired by Schwann cell remyelination (1991) Ann NY Acad Sci, 633, pp. 615-616Weller, R.O., Pathology of multiple sclerosis (1985) Mc Alpine's multiple sclerosis, pp. 301-343. , Matthews WB, Acheson ED, Batchelor Jr (eds.). Edinburgh: Churchill LivingstoneHsu, S.-M., Raine, L., Fanger, H., A comparative study of the peroxidase-antiperoxidase method and an avidin-biotin complex method for studying polypeptide hormones with radioimmunoassay antibodies (1981) Am J Clin Pathol, 75, pp. 734-738Majno, G., Palade, G.E., Studies on inflammation: I. The effect of histamine and serotonin on vascular permeability. An electron microscope study (1961) J Biophys Biochem Cytol, 11, pp. 571-605Reynolds, R., Wilkin, G.P., Cellular reaction to an acute demyelinating/ remyelinating lesion of the rat brainstem: Localization of GD3 ganglioside immunoreactivity (1993) J Neurosc Res, 36, pp. 405-42

Delayed Schwann cell and oligodendrocyte remyelination after ethidium bromide injection in the brainstem of Wistar rats submitted to streptozotocin diabetogenic treatment

Schwann cell disturbance followed by segmental demyelination in the peripheral nervous system occurs in diabetic patients. Since Schwann cell and oligodendrocyte remyelination in the central nervous system is a well-known event in the ethidium bromide (EB) demyelinating model, the aim of this investigation was to determine the behavior of both cell types after local EB injection into the brainstem of streptozotocin diabetic rats. Adult male Wistar rats received a single intravenous injection of streptozotocin (50 mg/kg) and were submitted 10 days later to a single injection of 10 µL 0.1% (w/v) EB or 0.9% saline solution into the cisterna pontis. Ten microliters of 0.1% EB was also injected into non-diabetic rats. The animals were anesthetized and perfused through the heart 7 to 31 days after EB or saline injection and brainstem sections were collected and processed for light and transmission electron microscopy. The final balance of myelin repair in diabetic and non-diabetic rats at 31 days was compared using a semi-quantitative method. Diabetic rats presented delayed macrophage activity and lesser remyelination compared to non-diabetic rats. Although oligodendrocytes were the major remyelinating cells in the brainstem, Schwann cells invaded EB-induced lesions, first appearing at 11 days in non-diabetic rats and by 15 days in diabetic rats. Results indicate that short-term streptozotocin-induced diabetes hindered both oligodendrocyte and Schwann cell remyelination (mean remyelination scores of 2.57 ± 0.77 for oligodendrocytes and 0.67 ± 0.5 for Schwann cells) compared to non-diabetic rats (3.27 ± 0.85 and 1.38 ± 0.81, respectively)