Found the article. Here is an exerpt. Almost says, "Hey, birth trauma is
counteracted by increased bili levels". What do you think?Role of heme
oxygenase-1 in hypoxia-reoxygenation: requirement of substrate heme to
promote cardioprotection.

Foresti R, Goatly H, Green CJ, Motterlini R.

Vascular Biology Unit, Department of Surgical Research, Northwick Park
Institute for Medical Research, Harrow HA1 3UJ, United Kingdom.

Heme oxygenase-1 (HO-1) catalyzes the enzymatic degradation of heme to
carbon monoxide, bilirubin, and iron. All three products possess biological
functions; bilirubin, in particular, is a potent free radical scavenger of
which its antioxidant property is enhanced at low oxygen tension. Here, we
investigated the effect of severe hypoxia and reoxygenation on HO-1
expression in cardiomyocytes and determined whether HO-1 and its product,
bilirubin, have a protective role against reoxygenation damage. Hypoxia
caused a time-dependent increase in both HO-1 expression and heme oxygenase
activity, which gradually declined during reoxygenation. Reoxygenation of
hypoxic cardiomyocytes produced marked injury; however, incubation with
hemin or bilirubin during hypoxia considerably reduced the damage at
reoxygenation. The protective effect of hemin is attributable to increased
availability of substrate for heme oxygenase activity, because hypoxic
cardiomyocytes generated very little bilirubin when incubated with medium
alone but produced substantial bile pigment in the presence of hemin.
Interestingly, incubation with hemin also maintained high heme oxygenase
activity levels during the reoxygenation period. Reactive oxygen species
generation was enhanced after hypoxia, and hemin and bilirubin were capable
once again to attenuate this effect. These results indicate that the HO-1-
bilirubin pathway can effectively defend hypoxic cardiomyocytes against
reoxygenation injury and highlight the issue of heme availability in the
cytoprotective action afforded by HO-1.

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