Albumin, among other molecules, binds and detoxifies
endotoxin in healthy people. Oxidative stress leads to
protein oxidation and thus to the impaired binding properties of
albumin. This property, in combination with increased gut permeability, leads to the appearance of
endotoxin in the systemic circulation and to impaired organ function. We hypothesize that these processes occur in the serum of
brain-dead organ donors.
Endotoxin was determined with an adapted Limulus
amoebocyte lysate assay. The
albumin fractions and binding capacity were determined by high-performance liquid chromatography (HPLC). FlowCytomix (eBioscience, San Diego, Calif) was used to determine the
cytokine levels. Carbonylated
proteins (CPs) and
myeloperoxidase (MPO) were measured by an
enzyme-linked
immunosorbent assay (ELISA). Eighty-four
brain-dead organ donors were enrolled and categorized by the duration of intensive care unit (ICU) stay. The
albumin-binding capacity for
dansylsarcosine was reduced in
brain-dead patients compared with controls.
Endotoxin positivity in 16.7% of donors was associated with decreased binding capacity in donors and worse survival of recipients. The CP and MPO levels of organ donors were significantly higher than in healthy controls. The durations of ICU stay increased
albumin oxidation. In addition,
interleukin-6 (IL-6),
IL-8,
IL-10, and IL-1β levels were increased in patients, whereas the
interferon-γ (IFN-γ) levels were within the normal range. We conclude that oxidative stress and systemic
endotoxemia are present in
brain-dead organ donors, which might affect recipient survival. High
endotoxin levels might be caused by increased gut permeability and decreased binding capacity of
albumin influenced not just by higher
albumin oxidation.