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Jayanti et al. Neuroimmunol Neuroinflammation 2020;7:92-108 I http://dx.doi.org/10.20517/2347-8659.2019.14 Page 93

Figure 1. Bilirubin & pathological conditions. Representation of the known CNS and not-CNS diseases where TSB is altered. For references
[3]
[2]
of CNS-diseases, see text. For details on not-CNS diseases, see references (according to Gazzin et al. and Wagner et al. )
elimination through urine and feces. Increased level of bilirubin (UCB and CB) in the blood is a
well-recognized marker of hepatic damage. Recently, slightly elevated serum bilirubin concentration
[1]
emerged as a biomarker of resistance versus chronic diseases . Epidemiological data have revealed
a reduced prevalence of type 2 diabetes, obesity and metabolic syndrome, certain cancers, and
especially cardiovascular diseases and related causes of mortality in Gilbert’s syndrome patients,
showing mild hyperbilirubinemia [2,3] [Figure 1]. The effect of the pigment has been demonstrated
to be due mainly to the unconjugated (or indirect) moiety of bilirubin (UCB). UCB, especially
in its free form [free bilirubin (Bf), the portion of UCB exceeding the serum albumin binding
capacity], enters tissues from blood, acting as a powerful antioxidant molecule at nanomolar
[4]
concentrations, where it is able to counteract 10,000 times higher levels of hydrogen peroxide (H O ) .
2
2
This capability has been related to the UCB-biliverdin cycle [Figure 2], which is able to regenerate the
pigment consumed by oxidants and acts complementary to cellular glutathione (GSH) . In the last years,
[4-6]