This study was aimed to evaluate and characterize the relationship between liver flukes infection of dicrocoeliosis, which can cause pathology and oxidative stress mechanism as a mediator of tissue damage concurrent with dicrocoeliosis infection.
Compared with fasciolosis, dicrocoeliosis produces mild symptoms in affected animals, however it causes severe economic losses, in terms of milk and meat production, due to liver function impairment. The disease can be fatal on rare occasions 17. Small ruminant dicrocoeliosis is common in sheep flocks with a prevalence of up to 100% in many European and Eastern countries 18.
The young flukes migrate directly up the biliary duct system of the liver without penetrating the gut wall, liver capsule or liver parenchyma as in fasciolosis. Clinical symptoms are not usually manifested, even in heavy infections, and therefore major lesions, due to liver impairment are detectable only at necroptic examination of the liver 1. Animals suffering from dicrocoeliosis may show anemia, oedema, emaciation, and in advanced cases, cirrhosis, scarring of the liver surface, and marked distension of bile ducts. Due to its buccal stilets, the small liver fluke irritates the bile duct surface, thus, causing proliferation and changes in the septal bile ducts of the lobular hepatic edges 17.
Although there were no detect any oxidative response in some parasite infections including G. intestinalis, T. saginata and B. hominis 12,13,14 we detected oxidative stress and lipid peroxidation at sheep naturally infected with D.dendriticum by measuring of MDA levels at sera.
MDA (lipid peroxidation) is a well-established mechanism of cellular injury and is used as an indicator of oxidative stres in cells and tissues 19. Oxidative stress and enhanced lipid peroxidation have been associated with several models of liver injury 20 and tissue injury in dicrocoeliosis might in part be mediated by the generation of reactive oxygen species 21.
In lamb liver, experimental fasciolosis induces a simultaneous increase in cytosolic calcium and a decrease in cytosolic glutathione by 8 weeks post-infection (p.i), when the liver-cell degenerative process is maximal 22. Similar alterations are detected in rats at 3 and 6 weeks p.i. such an oxidative cell injury has been suggested to occur in the course of fasciolosis as the consequence of tissue destruction produced by toxic secretions of the flukes 23.
Chronic inflammation may be related to oxidative alterations. In particular, the antioxidant defence capability of the liver, in hamsters experimentally infected with Dicrocoelium metacerceria, was increased 80-120 days p.i. In the meantime, a decrease in superoxide dismutase activity in both the cytosol and mitocondria was registered, indicating inefficient scavenging of reactive oxygen, leading to oxidative liver damage and an increase in alanin transaminase and aspartate transaminase activities 21. Sanchez-Compos et al. 21 suggested that expe-rimental dicrocoeliosis also courses with oxidative stress and lipid peroxidation as indica-ted by the significant increase in liver thio-barbituric acid-reactive subtances concent-ration. Lipid peroxidation resulting from oxidative stress produces MDA which forms DNA adducts and may cause cytotoxic effects 24.
Kargın and Fidancı 15, determined that there was a positive correlation between the intensity of the oxidative stress and the damage and kidney disease. In this study also we detected a relation between lipid peroxidation and liver damage due to the dicrocoeliosis in sheep.
Levels of MDA were significantly increased in sheep infected with D.dendriticum. The results of our study strongly suggested that one of the main reasons for high MDA levels in sheep infected with D.dendriticum could be decreased activity of defense system protecting tissue from free radicals damage.
The presence of lipid peroxidation could contribute to hepatic injury and to the reduced capacity for handling of drugs and xenobiotics previously reported for this parasitosis 25.
As it is known that lipid peroxidation is a free radical-related process and may occur biological systems under enzymatic control, e.g., for the generation of lipid-derived inflammatory mediators, or non-enzymatically. This later form was associated mostly with liver damage as a result of oxidative stress, which also involved cellular antioxidants in this process. The high MDA concentration and the significant correlation strongly indicate the occurence of antioxidative stress and lipid peroxidation as a mechanism of liver damage in cases of D.dendriticum infection.
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