Dynamics of Hepatic Melanogenesis in Newts in Recovery Phase from Hypoxia

The liver of lower vertebrates produces considerable amounts of molecular oxygen during hypoxia, thus the return to normoxic conditions initially brings on high values of oxygen saturation (sO2) in even venous blood. This temporary 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 normoxia, 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.