@article{3052827,
    title = "Liver metallothionein expression in thioacetamide-intoxicated rats",
    author = "Theocharis, SE and Margeli, AP and Karandrea, DN and Tsarpalis, KS and and Agapitos, EV and Spiliopoulou, CA and Koutselinis, AS",
    journal = "PATHOLOGY RESEARCH AND PRACTICE",
    year = "2000",
    volume = "196",
    number = "5",
    pages = "313-319",
    publisher = "ELSEVIER GMBH, URBAN & FISCHER VERLAG",
    issn = "0344-0338",
    doi = "10.1016/S0344-0338(00)80061-8",
    keywords = "metallothionein; liver; thioacetamide; injury; regeneration",
    abstract = "Metallothioneins (MT, a group of ubiquitous low molecular weight
proteins, implicated primarily in metal ion detoxification, are known to
be expressed during hepatocellular proliferation after partial
hepatectomy ill rats. In the present study, we investigated the
expression of MT in a rat model of liver injury and regeneration,
induced by intraperitoneal administration of ee thioacetamide (TAA), The
animals were killed at 0, 12, 24, 36, 48, 60, 72, 84, 96, 108 and 120
hours after TAA administration. The rate of tritiated thymidine
incorporation into hepatic DNA, the enzymatic activity of thymidine
kinase, and the assessment of the mitotic index in hepatocytes were used
as indices of liver regeneration. Liver MTs were detected
immunohistochemically. TAA administration caused severe hepatic injury,
followed by regeneration, MT expression became prominent in hepatocytes
as early as 12 hours post-TAA administration, At 24 and 36 hours
post-TAA administration intense nuclear and cytoplasmic staining of
hepatocytes was found in the vicinity of necrotic areas. The maximal
nuclear and cytoplasmic MT expression coincides with the peak of
hepatocyte proliferative capacity, occurring at 48 and 60 hours post-TAA
administration. MT expression correlated positively with the Zn content
of liver tissue, but negatively with serum one, at the time of maximum
hepatocyte proliferative capacity. This study suggests that MT
participates in hepatocyte replication after toxin-induced liver injury."
}