Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2001-5-29
pubmed:abstractText
Due to the widespread use of anthracyclines as antitumor agents, a large number of investigations have been reported analyzing clinical and molecular aspects of these quinone antibiotics. While the high affinity of anthracyclines towards chromosomal DNA has been held responsible for their antitumor activity, an increasing amount of data is being accumulated showing that these drugs also target mitochondria thus interfering with major mitochondrial functions. Since this toxicity of anthracyclines towards mitochondria is associated with side effects significantly limiting their chemotherapeutic dose, the corresponding underlying mechanisms need to be understood. Bioenergetic failure, enzyme inhibitions, lipid peroxidations, induction of membrane disorders as well as the initiation of oxidative stress are being attributed to the accumulation of anthracyclines at or inside mitochondria. In this review the wide spectrum of possible mode of actions of these antibiotics leading to mitochondrial dysfunctions will be presented and discussed.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0169-409X
pubmed:author
pubmed:issnType
Print
pubmed:day
2
pubmed:volume
49
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
87-105
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Mitochondria as subcellular targets for clinically useful anthracyclines.
pubmed:affiliation
Group Drug Targeting, Max-Delbrueck-Center for Molecular Medicine, Robert Roessle Strasse 10, D-13125 Berlin, Germany.
pubmed:publicationType
Journal Article, Review