Campesi, Ilaria and Straface, Elisabetta and Occhioni, Stefano and Montella, Andrea Costantino Mario and Franconi, Flavia (2013) Protein oxidation seems to be linked to constitutive autophagy: a sex study. Life sciences, Vol. 93 (4), p. 145-152. ISSN 0024-3205. eISSN 1879-0631. Article.
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Aim: Although constitutive autophagy is linked to redox state and participates in cell homeostasis, it is scarcely known if redox state, autophagy, and lysosomal function depend on sex, a factor that largely influences
health and diseases. Therefore, we evaluated the existence of sex differences in redox state and constitutive
autophagy in rat tissues.
Main methods: 7 week old Sprague–Dawley rats were used to obtain organs. Malondialdehyde (MDA), and
carbonylated proteins were measured by spectrophotometric methods for redox state assessment. The autophagy
biomarkers Beclin-1, and microtubule-associated protein 1 light chain 3 (LC3), the mammalian target of rapamycin (mTOR; checkpoint in autophagic process), and the lysosomal associated membrane protein (LAMP-1; biomarker of lysosomes) were evaluated by Western blotting. Immunofluorescence analysis was also performed for LC3 and LAMP-1 colocalization.
Key findings: In the heart, Beclin-1, and LC3-II/LC3-I were higher in males than in females suggesting that the
male heart has a major constitutive autophagy and this was linked with higher levels of carbonyl groups, indicating
that protein oxidation could play a role. In the liver, it was found that LAMP-1 was higher in males and greatly colocalized with LC3 indicating a larger number of autophagolysosomes. None of the above parameters was significantly different in the kidneys of both sexes with the exception of MDA, which was significantly higher in females.
Significance: The above results suggest that sex differences exist in redox state and autophagy and they occur in an organ-specific way. Importantly, it seems that the protein oxidation is more linked with constitutive autophagy, at least in cardiac ventricles, in comparison with lipid peroxidation.
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