TY - JOUR
T1 - Exposure to 1-bromopropane induces microglial changes and oxidative stress in the rat cerebellum
AU - Subramanian, Kaviarasan
AU - Mohideen, Sahabudeen Sheik
AU - Suzumura, Akio
AU - Asai, Naoya
AU - Murakumo, Yoshiki
AU - Takahashi, Masahide
AU - Jin, Shijie
AU - Zhang, Lingyi
AU - Huang, Zhenlie
AU - Ichihara, Sahoko
AU - Kitoh, Junzoh
AU - Ichihara, Gaku
N1 - Funding Information:
We are grateful to the Japan Society for the Promotion of Science (JSPS) for supporting the first author of this study, as a JSPS Post-doctoral Fellow at Nagoya University Graduate School of Medicine, Japan.
PY - 2012/12/8
Y1 - 2012/12/8
N2 - 1-Bromopropane (1-BP), an alternative to ozone-depleting solvents, is reported to exhibit neurotoxicity and reproductive toxicity in animals and humans. However, the underlying mechanism of the toxicity remains elusive. This study was designed to identify the microglial changes and oxidative stress in the central nervous system (CNS) after 1-BP exposure. Four groups of Wistar-ST rats (n=. 12 each) were exposed to 0, 400, 800 and 1000. ppm of 1-BP, 8. h/day for 28 consecutive days. The cerebellum was dissected out in 9 rats of each group and subjected to biochemical analysis, while the brains of the remaining 3 rats were examined immunohistochemically. Exposure to 1-BP increased the levels of oxidative stress markers [thiobarbituric acid reactive substances (TBARS), protein carbonyl and reactive oxygen species (ROS)] in a dose-dependent manner. Likewise, there was also 1-BP dose-dependent increase in nitric oxide (NO) and dose-dependent decrease in protein concentrations in the cerebellum. Immunohistochemical studies showed 1-BP-induced increase in cd11b/c-positive microglia area in the white matter of the cerebellar hemispheres. The results showed that exposure to 1-BP induced morphological change in the microglia and oxidative stress, suggesting that these effects are part of the underlying neurotoxic mechanism of 1-BP in the CNS.
AB - 1-Bromopropane (1-BP), an alternative to ozone-depleting solvents, is reported to exhibit neurotoxicity and reproductive toxicity in animals and humans. However, the underlying mechanism of the toxicity remains elusive. This study was designed to identify the microglial changes and oxidative stress in the central nervous system (CNS) after 1-BP exposure. Four groups of Wistar-ST rats (n=. 12 each) were exposed to 0, 400, 800 and 1000. ppm of 1-BP, 8. h/day for 28 consecutive days. The cerebellum was dissected out in 9 rats of each group and subjected to biochemical analysis, while the brains of the remaining 3 rats were examined immunohistochemically. Exposure to 1-BP increased the levels of oxidative stress markers [thiobarbituric acid reactive substances (TBARS), protein carbonyl and reactive oxygen species (ROS)] in a dose-dependent manner. Likewise, there was also 1-BP dose-dependent increase in nitric oxide (NO) and dose-dependent decrease in protein concentrations in the cerebellum. Immunohistochemical studies showed 1-BP-induced increase in cd11b/c-positive microglia area in the white matter of the cerebellar hemispheres. The results showed that exposure to 1-BP induced morphological change in the microglia and oxidative stress, suggesting that these effects are part of the underlying neurotoxic mechanism of 1-BP in the CNS.
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U2 - 10.1016/j.tox.2012.07.006
DO - 10.1016/j.tox.2012.07.006
M3 - Article
C2 - 22824114
AN - SCOPUS:84865990410
SN - 0300-483X
VL - 302
SP - 18
EP - 24
JO - Toxicology
JF - Toxicology
IS - 1
ER -