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dc.contributor.authorPesonen, Maija
dc.contributor.authorVähäkangas, Kirsi
dc.date.accessioned2019-04-10T07:06:45Z
dc.date.available2019-04-10T07:06:45Z
dc.date.issued2019
dc.identifier.urihttps://erepo.uef.fi/handle/123456789/7532
dc.description.abstractAutophagy is a catabolic pathway, which breaks down old and damaged cytoplasmic material into basic biomolecules through lysosome-mediated digestion thereby recycling cellular material. In this way, autophagy prevents the accumulation of damaged cellular components inside cells and reduces metabolic stress and toxicity. The basal level of autophagy is generally low but essential for maintaining the turnover of proteins and other molecules. The level is, however, increased in response to various stress conditions including chemical stress. This elevation in autophagy is intended to restore energy balance and improve cell survival in stress conditions. However, aberrant and/or deficient autophagy may also be involved in the aggravation of chemical-caused insults. Thus, the overall role of autophagy in chemical-induced toxicity is complex and only a limited number of environmental chemicals have been studied from this point of view. Autophagy is associated with many of the chemical-caused cytotoxic mechanisms, including mitochondrial dysfunction, DNA damage, oxidative stress, changes in the endoplasmic reticulum, impairment of lysosomal functions, and inflammation. This mini-review describes autophagy and its involvement in the responses to some common environmental exposures including airborne particulate matter, nanoparticles and tobacco smoke as well as to some common single environmental chemicals.
dc.language.isoenglanti
dc.publisherElsevier BV
dc.relation.ispartofseriesToxicology letters
dc.relation.urihttp://dx.doi.org/10.1016/j.toxlet.2019.01.007
dc.rightsCC BY-NC-ND 4.0
dc.subjectautophagosome
dc.subjectpesticides
dc.subjectparticulate matter
dc.subjectnanoparticles
dc.subjecttobacco smoke
dc.titleAutophagy in exposure to environmental chemicals
dc.description.versionfinal draft
dc.contributor.departmentA.I. Virtanen -instituutti
dc.contributor.departmentSchool of Pharmacy, Activities
uef.solecris.id60167139en
dc.type.publicationTieteelliset aikakauslehtiartikkelit
dc.relation.doi10.1016/j.toxlet.2019.01.007
dc.description.reviewstatuspeerReviewed
dc.format.pagerange1-9
dc.publisher.countryAlankomaat
dc.relation.issn0378-4274
dc.relation.volume305
dc.rights.accesslevelopenAccess
dc.type.okmA2
uef.solecris.openaccessEi
dc.rights.copyright© Elsevier B.V.
dc.type.displayTypearticleen
dc.type.displayTypeartikkelifi
dc.rights.urlhttps://creativecommons.org/licenses/by-nc-nd/4.0/


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