Literature DB >> 3361301

Altered cerebral protein turnover in rats following prolonged in vivo treatment with nicotine.

S S Katyare1, J M Shallom.   

Abstract

Turnover rates of cerebral proteins were examined in control adult rats and in those subjected to prolonged in vivo treatment with "low" (0.02 mg/ml) or "high" (0.04 mg/ml) doses of nicotine (added to drinking water), using [14C]bicarbonate as the label. It was found that the turnover of proteins in various subcellular fractions consisted of two distinct components turning over at a "fast" or a "slow" rate and having relatively short or long half-lives, respectively. Thus in control animals the half-lives of the protein components turning over at a fast rate ranged from 1.31 to 3.61 days whereas for those turning over at a slow rate the half-lives ranged from 8.56 to 24.28 days. Treatment with low doses of nicotine resulted in a more rapid turnover of nuclear fast turning over component with a concomitant decreased turnover of homogenate, cytosol, mitochondrial, and microsomal proteins; in the synaptosomal membranes this component disappeared altogether. The half-lives of the slow turning over components decreased in general from 14.3 to 33.3% with the exception of the nuclear proteins, where the half-live increased by 71.1%. Turnover of microsomal proteins was not affected. When the animals were given a high dose of nicotine, the turnover of fast components became even more rapid for nuclear, myelin, and microsomal proteins with a decrease in half-life from 26.6 to 32.3%. By contrast, half-lives of synaptosomal and mitochondrial proteins increased by 16.1-89.3%. These changes were not reflected in the turnover rate of whole homogenate proteins.(ABSTRACT TRUNCATED AT 250 WORDS)

Entities:  

Mesh:

Substances:

Year:  1988        PMID: 3361301     DOI: 10.1111/j.1471-4159.1988.tb03016.x

Source DB:  PubMed          Journal:  J Neurochem        ISSN: 0022-3042            Impact factor:   5.372


  7 in total

Review 1.  Mechanisms of soft and hard electrophile toxicities.

Authors:  Richard M LoPachin; Brian C Geohagen; Lars U Nordstroem
Journal:  Toxicology       Date:  2019-02-28       Impact factor: 4.221

2.  Role of the Nrf2-ARE pathway in acrylamide neurotoxicity.

Authors:  Lihai Zhang; Terrence Gavin; David S Barber; Richard M LoPachin
Journal:  Toxicol Lett       Date:  2011-04-21       Impact factor: 4.372

3.  Thyroid hormone treatments differentially affect the temperature kinetics properties of FoF1 ATPase and succinate oxidase as well as the lipid/phospholipid profiles of rat kidney mitochondria: a correlative study.

Authors:  Hiren R Modi; Samir P Patel; Surendra S Katyare; Minal Patel
Journal:  J Membr Biol       Date:  2007-06-14       Impact factor: 1.843

4.  Significant modulation of mitochondrial electron transport system by nicotine in various rat brain regions.

Authors:  Ju Wang; Jong-Man Kim; David M Donovan; Kevin G Becker; Ming D Li
Journal:  Mitochondrion       Date:  2009-01-30       Impact factor: 4.160

Review 5.  Molecular mechanisms of the conjugated alpha,beta-unsaturated carbonyl derivatives: relevance to neurotoxicity and neurodegenerative diseases.

Authors:  Richard M LoPachin; David S Barber; Terrence Gavin
Journal:  Toxicol Sci       Date:  2007-12-13       Impact factor: 4.849

6.  Genome-wide expression analysis reveals diverse effects of acute nicotine exposure on neuronal function-related genes and pathways.

Authors:  Ju Wang; Wenyan Cui; Jinxue Wei; Dongxiao Sun; Ramana Gutala; Jun Gu; Ming D Li
Journal:  Front Psychiatry       Date:  2011-03-08       Impact factor: 4.157

Review 7.  Molecular mechanism of acrylamide neurotoxicity: lessons learned from organic chemistry.

Authors:  Richard M LoPachin; Terrence Gavin
Journal:  Environ Health Perspect       Date:  2012-10-11       Impact factor: 9.031

  7 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.