Lectin-like oxidized low-density lipoprotein (LDL) receptor (LOX-1)-mediated pathway and vascular oxidative injury in older-age rat renal transplants

Abstract

Induction of LOX-1-related oxidation pathways and increased susceptibility to oxidative stress could play an important role in promoting vascular injury in old renal transplants independent of the recipient age.

Hydroethidine- and MitoSOX-derived red fluorescence is not a reliable indicator of intracellular superoxide formation: Another inconvenient truth

“…Examples of the use of HE in ex vivo experiments include the detection of in situ production of superoxide in brain tissue [53,164-173], spinal cord sections[174-176], blood vessels [74,91,138,139,141,145,177-270], diaphragms [52,85,271-273], various components of kidney [94,274-280], heart [201,281-291], islets of Langerhans [292], penis sections [293], liver sections [294,295], lungs [296,297], retinal tissue sections [298], eye sections [299-301] and prostate tissue [302]. HE has been also used to detect superoxide in tissue homogenates [207,279,303-306] as well as in whole blood [307-311].…”

Halogenation Activity of Mammalian Heme Peroxidases

“…(iii) Cotreatment with amiodarone, an antiarrhythmic medication, after a 10 h treatment led to massive accumulation of HOCl-modified epitopes [239] that could be reduced to baseline levels by either rabbit antineutrophil antiserum or heparin. Colocalization of chlorinated epitopes with lectin-like oxidized LDL receptor-1 during the initiation of transplant vascular injury in rats [240] is supported by data that the lectin-like oxidized LDL receptor-1 acts as a receptor for HOCl-modified lipoproteins [241,242]. Most importantly, high oral dosing with SCN − , a competitive MPO substrate, protected against myocardial ischemia/reperfusion injury in male Sprague Dawley rats by impairing infarct size and decreasing mAb recognition of HOCl-damaged myocardial proteins generated via the MPO-H 2 O 2 -Cl − system of activated neutrophils [243].…”