Abstract
Background: “Kernicterus” historically describes the unconjugated bilirubin (UCB) accumulation in selective brain regions, leading to neurological damage in hyperbilirubinemic newborn babies and in Crigler-Najjar type I patients. Hyperbilirubinemic (jj) Gunn rats develop neurological deficits that parallels the human pathology and a similar pattern of regional brain UCB distribution under displacing agents treatment. Aims: Methods: Cortex (Cx), superior collicula (SC), inferior collicula (IC), cerebellum (CLL) and the rest of the brain (RB) were collected 1, 6, 24, 48 and 72 hrs after injection of sulfadimethoxine (200 mg/Kg; IP) in 17 days-old jj animals and in not treated JJ, Jj and jj rats. TUCB was analyzed by the HPLC based method (Zelenska_2008). Results: In untreated jj animals TUCB brain amounts was about 80 times higher than in Jj and JJ, and no regional differences were detected. After sulphadimethoxine administration TUCB picked differently in the regions analyzed: 1 hr in Cx and SC, 6 hrs in RB, 24 hrs in IC, 6 - 24 hrs in CLL. 72 hrs after injection, TUCB content was lower than in not treated littermates. Conclusions: The differential entry and clearance across brain areas show regional difference in cellular mechanisms modulating tissue UCB concentration. The different kinetics might be involved in the tissue resistance/sensitivity to bilirubin toxicity of nervous system.
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