Organohalogen concentrations and a gross and histologic ...

152
Mononuclear cell infiltrations and lipid granulomas
Mononuclear cell infiltrates - accompanied by fibrosis – might be reactions
due to local depositioning of bacteria, virus or injury of local blood vessels
(MacLachlan and Cullen 1995). The strong indications of predispositioning
of lipid granulomas around swollen Ito-cells, located in the narrow space of
Disse and between hepatocytes, might be explained by infectious agens
originating from the blood supply, leading to random focal necroses (burst
of Ito-cells) (Ibid.).
Portal fibrosis and bile duct proliferation
Age related portal fibrosis due to chronic infections (cholangitis and biliary
obstruction) is a common feature in mammals (MacLachlan and Cullen
1995) and it has been reported in the romanian brown bear (U. arctos) (Prunescu
et al., 2003) and Arctic beluga whales (Delphinapterus leucas) (Woshner
et al., 2002). In Prunescu et al.,’s study, seasonal liver fibrosis (highest in
spring) of the hepatic venous system was shown, and they speculated
whether this was due to pre-hibernation physiological adaptations (Ibid.).
This finding was in agreement with our study, although only pregnant polar
bears den for a long time, whereas all other polar bears of both sexes and age
only now and then use shelters (faculative dens), when environmental conditions
are adverse (e.g. Ferguson et al., 2000). Bile duct proliferation due to
hepatic injury has been related to liver injury and is as such a non-specific
histopathological change also described in Arctic beluga whales (Delphinapterus
leucas) (MacLachlan and Cullen 1995, Wosher et al., 2002). The aetiology
of chronic lymphocytic cholangitis is unknown but toxic injury, parasitism
or periductular fibrosis has been proposed (MacLachlan and Cullen
1995).
Histology and contaminants
To our knowledge, liver histology in relation to environmental levels of organohalogens
has only been studied in cormorants (Phalacrocorax carbo)
(Fabczak et al., 2000) and fish (Abramis brama) (Koponen et al., 2001) but not
in mammals. Therefore it is hard to evaluate the relationship between liver
histology and chronic exposure to environmental levels of organohalogen
compounds in the East Greenland polar bear. Liver toxic substances (e.g.
copper, pyrrolizidine alkaloids, carbon tetrachloride and phytotoxins) usually
produce a centrolobulary (periacinary) zone 3 characteristic injury due
to the low oxygen gradient (hypoxia) and high concentrations of e.g. Cyt-
P450 isozymes (activation of reactive metabolites) of this zone (MacLachlan
and Cullen 1995, Parkinson 1996). In the case of hepatocytic and Ito-cell fat
accumulation in our study, these were often concentrated centrolobularily or
centroacinary, respectively. Abnormal amounts of fat is known to be accumulated
in the liver during high lipid ingestion, starvation, abnormal hepatocytic
function, excessive dietary intake of carbohydrates and decreased
syntheses of apoproteins and thereby lipoproteins (Ibid.). Hence the large
content of lipids in polar bear livers could be a function of hyperphagia and
starvation due to seasonal changes in food resources as discussed in previous
sections. However, acute toxic investigations in laboratory rats of PCBs,
DDTs and dieldrin have shown to induce high lipid accumulation - probably
due to decreased production of lipoproteins through impaired ATP synthesis
and protein synthesis – centrolobularily in hepatocytes (foamy cytoplasm
or large vacuoles) (e.g. Kimbrough et al., 1971, Kimbrough et al., 1972,
Bruckner et al., 1974, Bergman et al., 1992, MacLachlan and Cullen 1995, Par-