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Matrix metalloproteinases 2 and 9 in central nervous system and their modification after vanadium inhalation
Author(s) -
ColínBarenque L.,
MartínezHernández M. G.,
BaizaGutman L. A.,
AvilaCosta M. R.,
OrdóñezLibrado J. L.,
BizarroNevares P.,
RodriguezLara V.,
PiñónZarate G.,
RojasLemus M.,
MussaliGalante P.,
Fortoul T. I.
Publication year - 2008
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.1326
Subject(s) - piriform cortex , hippocampus , olfactory bulb , striatum , chemistry , endocrinology , oxidative stress , central nervous system , matrix metalloproteinase , medicine , pathology , dopamine , biochemistry
Vanadium (V) derivatives are well‐known environmental pollutants and its toxicity has been related with oxidative stress. Toxicity after vanadium inhalation on the substantia nigra, corpus striatum, hippocampus and ependymal epithelium was reported previously. The purpose of this study was to analyse the role of matrix metalloproteinases 2 (MMP‐2) and 9 (MMP‐9) in the changes observed in brain tissue after chronic V inhalation. Mice were exposed to vaporized, vanadium pentoxide 0.02 m in deionized water for 1 h twice a week, and killed at 1 h, 1, 2 and 4 weeks after exposure. The brain was removed and the olfactory bulb, prefrontal cortex, striatum and hippocampus were dissected and the MMP content was obtained by zymography. The results showed that MMP‐9 increased in all the structures at the end of the exposure, although in the hippocampus this increment was evident after 1 week of exposure. When MMP‐2 was analysed in the olfactory bulb and prefrontal cortex it remained unchanged throughout the whole exposure, while in the hippocampus it increased at week 4, while in the striatum MMP‐2 increased from the second week only, through the whole experiment. These results demonstrate that V increased MMPs in different structures of the CNS and this change might be associated with the previously reported modifications, such as dendritic spine loss and neuronal cell death. The modifications in MMPs could be related with blood–brain barrier (BBB) disruption which was reported previously. Oxidative stress might also be involved in the activation of these gelatinases as part of the different mechanisms which take place in V toxicity in the CNS. Copyright © 2007 John Wiley & Sons, Ltd.