Light and Electron Microscopic Observations in Nerve Cell Nucleolar Damage in Human Traumatic and Complicated Brain Injuries

  • Orlando Castejón Universidad del Zulia-Venezuela
Palabras clave: nucleolar damage, nerve cells, brain injury, light microscopy

Resumen

Objective: To study microscopically the nucleolar alterations induced by severe and complicated traumatic human head injuries using cortical biopsies taken during neurosurgical treatment. Material and methods: 10 cortical biopsies from different cortical regions were study by means of light microscopy, scanning-transmission electron microscopy, and transmission electron microscopy. Results: Pyramidal nerve cells examined with light microscopy thick sections, and scanning-transmission electron microscopy semithin sections exhibited apparent intact nucleolar structure, and ring-shaped nucleolar morphology. Ultrathin sections examined by transmission electron microscopy showed some populations of edematous non-pyramidal neurons exhibiting normal nucleolar substructure with well preserved subcompartments. Another groups of non-pyramidal neurons displayed a nucleolar homogenization process without distinction of nucleolar subcompartments. Other neuronal populations and perivascular astrocytes showed a frank nu- cleolar disassembly process. The nucleolar morphological alterations are discussed in relation with the traumatic brain injury, anoxic ischemic conditions of brain parenchyma, oxidative stress, calcium overload, glutamate and hemoglobin excitotoxicity, and caspase activation. Conclusion: The complicated traumatic brain injuries showed neuronal populations with apparent intact nucleolar structures, and other neuronal groups with homogenization, disassembly and fragmentation of nucleolar components.

Descargas

La descarga de datos todavía no está disponible.

Biografía del autor/a

Orlando Castejón, Universidad del Zulia-Venezuela
Profesor de la Universidad del Zulia

Citas

Annunziato, L.; Amoroso, S.; Pannacione, A, et al. (2003). Apoptosis induced in neuronal cells by oxidative stress: role played by caspases and intracellular calcium ions. Toxicol. Lett. 139: 125-133.

Castejón, O.J.; Castejón, H:V.; Diaz, M.; Castellano, A. (2001). Consecutive light microscopy, scanning-transmission electron microscopy and transmission electron microscopy of traumatic human brain oedema and ischaemic brain damage. Histol. Histopathol. 16:1117-1134.

Castejón, O.J. (2004). Nerve cell nuclear and nucleolar abnormalities in the human oedematous cerebral cortex. An electron microscopic study using cortical biopsies. J Submicrosc. Cytol. Pathol. 36: 273-283.

Castejón, O.J.; Arismendi, G.J. (2006). Nerve cell death types in the edematous human cerebral cortex. J. Submicrosc. Cytol. Pathol. 38: 21-36.

Castejón, OJ. (2008). Nerve cell nuclear and nucleolar abnormalities in the human edematous cerebral cortex. In: Electron microscopy of Human Brain Edema. Universidad del Zulia. Venezuela. pp 67-78.

Comal, I. (1999). The nucleolus: a paradigm for cell proliferation and aging. Brazilian J. Med. Biol. Res. 32: 1473-1478.

Daxnerova, Z.; Marsala, M.; Marsala, J. (1995). Graded postishemic reoxygenation attenuates ischemia-reperfusion-induced nuclear and nucleolar damage in lumbosacral dorsal root ganglia neurons. A light and electron microscopic study in rabbit. J. Hirnforsch. 36: 379-391.

Evans, P.H. (1993). Free radicals in brain metabolism and pathology. Brit. Med. Bull. (Suppl.) 493: 577-587.

Ginsberg, M.D.; Watson, B:D.; Bustos, R. (1988). Peroxidative damage to cell membranes following cerebral ischemia. A cause of ischemic brain injury. Neurochem. Pathol. 9: 171-173.

Jenkins, L.W.; Povlishock, J.T.; Lewelt, W.; Miller, J.D.; Becker, D.P. (1981). The role of ischemic recirculation on the development of ischemic neuronal injury following complete cerebral ischemia. Acta Neuropathol. (Berl). 55: 205-220.

Karamaris, E, Stefanis, L.; MacLaurin, J. et al. (2000). Involvement of caspase 3 in apoptotic death of cortical neurons. Mol. Cell Neurosci. 15: 368-379.

Kastner, P.; Mosgoeller, W.; Fang-Kircher, S. et al. (2003). Deficient brain RNA polymerase and altered nucleolar structure persists until day 8 after perinatal asphyxia of the rat. Pediatr. Res. 53: 62-71.

McKeage, M.; Hsu, T.; Screnci, D.; Haddad, G.; Baquley, B.C. (2001). Nucleolar damage correlates with neurotoxicity induced by different platinum drugs. Br. J. Cancer 85: 1920-1925.

Morley, P.; Tauskela, J.S.; Hakim, A:M: (1999). Cerebral Ischemia In: Walz W (Ed) Calcium Overload. New Jersey, Humana Press.pp 69-104.

Navacues, J.; Casafont, I.; Villagra, N.T.; Lafarga, M.; Berciano, M:T. (2004). Reorganization of nuclear components of type A neurons of trigeminal ganglion in response to inflammatory injury of peripheral nerve endings. J. Neurocytol. 33: 393-405.

Nicholls, D.G.; Budd, S.L.; Castillo, R.F.; Ward, M.W. (1999). Glutamate excitotoxicity and neuronal energy metabolism. Ann. NY Acad. Sci. 893:1-12.

Paschen, W. (1996). Glutamate excitotoxicity in transient global cerebral ischemia. Acta Neurobiol Exp (Wars) 56: 313-322.

Paschen, W. (2000). Role of calcium in neuronal cell injury: which subcellular compartment is involved? Brain Res. Bull. 53: 409-413.

Paschen, P.; Tauskela, J.S.; Hakim, A.M. (1999). Cerebral Ischemia In: WalzW (Ed). Calcium Overload. New Jersey, Humana Press. pp 69-104.

Raghupathi, R.; McIntosh, T.K.; Smith, D.H. (1995) Cellular responses to experimental brain injury. Brain Pathol. 5: 437-442.

Rasika, I.; Shaw, P.J.; Cmarko, D. (2006). New insights into nucleolar architecture and activity. Int. Rev. Cytol. 255: 177-235.

Schwarzacher, H.G.; Wachtler, F. (1993). The nucleolus. Anat. Embryol. 188: 515-536.

Siesjo, B.K.; Garia, C.D.; Bengtson, F. (1989). Free radicals and brain damage. Cerebrovasc. Brain Metab. Rev. 1: 165-171.

Soldani, C.; Bottone, M.G.; Pelliciari, C.; Scoyassi AI. (2006). Nucleolus disassembly in mitosis and apoptosis: dynamic redistribution of phosphorilated c- Mic, fibrillarin and K1-67. Eur. J Histochem. 50: 273-280.

Traystman, R.J.; Kirsch, J.R.; Koehler, R.C. (1991). Oxygen radical mechanisms of brain injury following ischemia and reperfusion. J. Appl. Physiol. 71: 1185-1195.

Trentani, A.; Testillano, P.S.; Risueno, M.C.; Biggiogera, M. (2003). Visualization of transcription sites at the electron microscope. Eur. J. Histochem. 47: 195-200.

Valero, J.; Berciano, M.T.; Weruana, E.; Lafarga, M.; Alonso, J.B. (2006). Predegeneration of mitral cells in the pcd mutant mouse is associated with DNA damage, transcriptional repression, and reorganization of nuclear speckles and Cajal bodies. Mol. Cell Neurosci. 33: 283-295.

Yakovlev, A.G.; Di, X.; Movsesyan, V.; et al. (2001). Presence of DNA fragmentation and lack of neuroprotective effect in DFF45 knockout mice subjected to traumatic brain injury. Mol. Med. 7: 205-216.

Zimber, A.; Nouvan, O:D.; Gespach. C. (2004) Nuclear bodies and compartment: functional roles and cellular signaling in health and disease. Cell Signal 16: 1085-1104.

Cómo citar
Castejón, O. (1). Light and Electron Microscopic Observations in Nerve Cell Nucleolar Damage in Human Traumatic and Complicated Brain Injuries. Revista De La Universidad Del Zulia, 2(3), 133-149. Recuperado a partir de https://produccioncientificaluz.org/index.php/rluz/article/view/12657