Although prion diseases, a group of fatal neurodegenerative diseases of human and animals, are presumed to be caused by several mechanisms including abnormal change of prion protein, oxidative stress is still believed to play a central role in development of the diseases. Cigarette smoking has a few...
Although prion diseases, a group of fatal neurodegenerative diseases of human and animals, are presumed to be caused by several mechanisms including abnormal change of prion protein, oxidative stress is still believed to play a central role in development of the diseases. Cigarette smoking has a few beneficial effects on neuronal diseases such as Alzheimer's disease and Parkinson's disease despite of many detrimental effects. In this study, we investigated how chronic cigarette smoking could exert such beneficial effect against oxidative damage. For this study, homogenates of 87V scrapie-infected brain was inoculated on intracerebral system of IM mice through stereotaxic microinjection and biochemical properties concerning with oxidative stress were examined. The scrapie infection decreased the activity of mitochondrial Mn-containing superoxide dismutase by 50% of the control, meanwhile the effects on other antioxidant enzymes including Cu or Zn-containing superoxide dismutase were not significant. Additionally, the infection elevated superoxide level as well as monoamine oxide-B (MAO-B) in the infected brain. Interestingly, many of the detrimental effects were improved in partial or significantly by long-term cigarette smoke exposure (CSE). CSE not only completely prevented the generation of mitochondrial superoxide but also significantly (p<0.05) decreased the elevated mitochondrial MAO-B activity in the infected brain. Concomitantly, CSE prevented subsequent protein oxidation and lipid peroxidation caused by scrapie infection; however, it did not affect the activities of antioxidant enzymes. These results suggest that chronic exposure of cigarette smoke contribute to in part preventing the progress of neurodegeneration caused by scrapie infection.
Although prion diseases, a group of fatal neurodegenerative diseases of human and animals, are presumed to be caused by several mechanisms including abnormal change of prion protein, oxidative stress is still believed to play a central role in development of the diseases. Cigarette smoking has a few beneficial effects on neuronal diseases such as Alzheimer's disease and Parkinson's disease despite of many detrimental effects. In this study, we investigated how chronic cigarette smoking could exert such beneficial effect against oxidative damage. For this study, homogenates of 87V scrapie-infected brain was inoculated on intracerebral system of IM mice through stereotaxic microinjection and biochemical properties concerning with oxidative stress were examined. The scrapie infection decreased the activity of mitochondrial Mn-containing superoxide dismutase by 50% of the control, meanwhile the effects on other antioxidant enzymes including Cu or Zn-containing superoxide dismutase were not significant. Additionally, the infection elevated superoxide level as well as monoamine oxide-B (MAO-B) in the infected brain. Interestingly, many of the detrimental effects were improved in partial or significantly by long-term cigarette smoke exposure (CSE). CSE not only completely prevented the generation of mitochondrial superoxide but also significantly (p<0.05) decreased the elevated mitochondrial MAO-B activity in the infected brain. Concomitantly, CSE prevented subsequent protein oxidation and lipid peroxidation caused by scrapie infection; however, it did not affect the activities of antioxidant enzymes. These results suggest that chronic exposure of cigarette smoke contribute to in part preventing the progress of neurodegeneration caused by scrapie infection.
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문제 정의
In this study, we investigated how chronic cigarette smoking could exert such beneficial effect against oxidative damage in scrapie infected animals model. For this study, homogenates of 87V scrapie-infected brain was inoculated on intracerebral system of IM mice through stereotaxic microinjection and biochemical properties concerning with oxidative stress were examined.
제안 방법
In this study, we investigated how chronic cigarette smoking could exert such beneficial effect against oxidative damage in scrapie infected animals model. For this study, homogenates of 87V scrapie-infected brain was inoculated on intracerebral system of IM mice through stereotaxic microinjection and biochemical properties concerning with oxidative stress were examined.
K). The mice were divided into four groups: control (C), scrapie-injected (P), control with exposure to cigarette smoke (CS), and scrapie-injected with exposure to cigarette smoke (PS). Twenty and thirty mice were used for each control (C and CS) and each scrapie-infected group (P and PS), respectively.
The samples were precipitated with 0.5of 20 % TCA, and centrifuged at 11,000 × g and 4℃ for 3The same procedure was repeated with 10% TCA for three times.
대상 데이터
Five mice were housed in each cage and supplied with water and food ad libitum in a clean conventional animal facility (22 ± 2 ℃, 50-60 % relative humidity, and 12 h light/dark cycle).
The mice were divided into four groups: control (C), scrapie-injected (P), control with exposure to cigarette smoke (CS), and scrapie-injected with exposure to cigarette smoke (PS). Twenty and thirty mice were used for each control (C and CS) and each scrapie-infected group (P and PS), respectively. Five mice were housed in each cage and supplied with water and food ad libitum in a clean conventional animal facility (22 ± 2 ℃, 50-60 % relative humidity, and 12 h light/dark cycle).
데이터처리
Statistical analysis was done by one-way ANOVA with a post hoc Duncan test. A value of p<0.
이론/모형
Contents of sulfhydryl compounds in brain cytosol were measured at 412 nm according to the procedure of Sedlak and Lindsay (1968) using 5,5’-dithiobis-2(2-nitrobenzoic acid) (DTNB) as a substrate.
Protein carbonyl content was measured by the method of Levine et al. (1990). Protein was precipitated with 20 % trichloroacetic acid (TCA).
The 10,000 x g pellet corresponding to the mitochondrial fraction, was resuspended with theHEPES buffer. Protein concentrations were determined by the method of Lowry et al. (1951) with bovine serum albumin as a standard. Aliquotes of cytosol and mitochondrial fractions were stored at -70℃ until use.
후속연구
In the present study, long-term exposure of cigarette smoke significantly attenuated ROS generation and oxidative stress caused by scrapie infection; the levels of MDA and protein carbonyl compounds were declined to normal conditions. Although further investigations are necessary to identify what kind of substances may be responsible, present results suggest the possibility that a substance(s) in cigarette smoke which are trapped into the physiological fluid at lung may circulate into the central nervous system and produce the biologically active species that protect neuronal functions against oxidative stress, in addition to plenty of oxidative substances.
These findings suggest that chronic exposure of cigarette smoke may partly contribute to suppression in the progress of neurodegeneration caused by scrapie infection. Further studies are necessary to establish the beneficial actionof cigarette smoke exposure against neurological diseases in mechanistic aspects.
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