Dynamics of Hepatic Melanogenesis in Newts in Recovery Phase from Hypoxia~!2008-11-17~!2008-12-01~!2009-01-26~!

Abstract

The liver of lower vertebrates produces considerable amounts of molecular oxygen during hypoxia, thus the re- turn to normoxic conditions initially brings on high values of oxygen saturation (sO2) in even venous blood. This tempo- rary hyperoxia triggers the oxidative process of hepatic melanogenesis. In newts rendered hypoxic by forced immersion, after 90 minutes of re-oxygenation sO2 of mixed blood drawn from the conus arteriosus reached 96±3% versus 84±7% in controls (P<0.05), whilst the percent of melanin in histological sections of the liver rose from 8.8±2.1 to 15.4±5.4% (P<0.01). Melanisation of the organ was caused by Kupffer cells which invaded the parenchyma from the subcapsular layer of myeloid tissue, became engorged with melanosomes, died and assumed a globular shape. After 6 hours of nor- moxia, sO2 values returned to normal and the dead cells had disappeared, but the cytoplasm of the surviving Kupffer cells exhibited fragments of residual bodies, membrane-bound clusters of undigested melanosomes.