Histopathologic analysis of hamster hepatocytes submitted to experimental infection with Leishmania donovani

• Published in: Parasitology research (1987) 2002-09, Vol.88 (9), p.829-836
• Main Authors: VIANNA, V. L. P, TAKIYA, C. M, DE BRITO-GITIRANA, L
• Format: Article
• Language: English
• Subjects: 3,3'-Diaminobenzidine - chemistry; Animals; Biological and medical sciences; Cricetinae; Experimental protozoal diseases and models; Hepatocytes - parasitology; Hepatocytes - pathology; Hepatocytes - ultrastructure; Histocytochemistry; Infectious Disease Transmission, Vertical; Infectious diseases; Leishmania donovani - growth & development; Leishmania donovani - isolation & purification; Leishmania donovani - pathogenicity; Leishmaniasis, Visceral - diagnosis; Leishmaniasis, Visceral - parasitology; Leishmaniasis, Visceral - pathology; Liver - cytology; Liver - pathology; Lysosomes - metabolism; Lysosomes - ultrastructure; Male; Medical sciences; Mesocricetus; Parasitic diseases; Peroxisomes - metabolism; Peroxisomes - ultrastructure; Protozoal diseases
• ISSN: 0932-0113; 1432-1955
• DOI: 10.1007/s00436-001-0577-0

Hepatocytes from different vertebrates are used increasingly as models of environmentally driven cell structure plasticity and for the investigation of ultrastructural pathological patterns induced by cell injury. The present study was carried out to assess the morphological changes in hamster hepatocytes subjected to chronic infection by amastigote forms of Leishmania donovani. Liver fragments were processed for routine light and transmission electron microscopy. For cytochemical visualization of peroxisomes, liver slices were incubated in alkaline 3,3'-diaminobenzidine (DAB) medium at pH 10.0. The results showed that the presence of Leishmania donovani induced distinct ultrastructural changes in the liver acinus (zone 2). The significant pathological changes in hepatocytes consisted of disruption of the endomembrane system and alterations of both the peroxisomal compartment and the distribution of hepatic glycogen. Particularly, hepatic peroxisomes exhibited different shapes and sizes, with modifications of the peroxisomal matrix, including absence of the catalase reaction. These observations suggest an adaptive response of hepatocytes, with cytological reorganization after parasitic infection. The presence of DAB-negative peroxisomes could be morphological evidence of a metabolic disturbance of this organelle. The parasitic infection, through deregulation of the cytokene network, is probably responsible for those structural alterations, since similar changes have been observed in vivo and in vitro.