2024-03-28T19:12:12Zhttp://uvadoc.uva.es/oai/requestoai:uvadoc.uva.es:10324/60772021-06-23T09:51:28Zcom_10324_1134com_10324_931com_10324_894col_10324_1213
Ganfornina Álvarez, María Dolores
Carmo, Sonia do
Lora, Jose M.
Torres Schumann, Sonia
Vogel, Marci
Allhorn, Maria
González, Constancio
Bastiani, Michael J.
Rassart, Eric
Sánchez Romero, Diego
2008
Producción Científica
Many nervous system pathologies are associated with
increased levels of apolipoprotein D (ApoD), a lipocalin
also expressed during normal development and aging.
An ApoD homologous gene in
Drosophila
, Glial Lazarillo,
regulates resistance to stress, and neurodegeneration in the
aging brain. Here we study for the first time the protective
potential of ApoD in a vertebrate model organism. Loss
of mouse ApoD function increases the sensitivity to
oxidative stress and the levels of brain lipid peroxidation,
and impairs locomotor and learning abilities. Human
ApoD overexpression in the mouse brain produces opposite
effects, increasing survival and preventing the raise of
brain lipid peroxides after oxidant treatment. These
observations, together with its transcriptional up-regulation
in the brain upon oxidative insult, identify ApoD as an acute
response protein with a protective and therefore beneficial
function mediated by the control of peroxidated lipids.
Key words: learning, lipid peroxidation, lipocalin, locomotor
behavior, paraquat, oxidative stress.
application/pdf
http://uvadoc.uva.es/handle/10324/6077
eng
Blackwell Publishing
Nervioso, sistema - Enfermedades
Lípidos
Apolipoprotein D is involved in the mechanisms regulating protection from oxidative stress
info:eu-repo/semantics/article
TEXT
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