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Cadmium-induced apoptosis in mouse liver
S S Habeebu1, J Liu, C D Klaassen
1Department of Pharmacology, Toxicology, and Therapeutics, University of Kansas Medical Center, Kansas City 66160-7417, USA.
Toxicology and Applied Pharmacology
|May 8, 1998
Summary
Cadmium exposure triggers apoptosis, a programmed cell death, in mouse livers, which precedes necrosis. This study details the timing and dose-dependency of apoptosis and necrosis in cadmium toxicity.
Area of Science:
- Toxicology
- Cell Biology
- Hepatology
Background:
- Acute hepatotoxicity of cadmium (Cd) is documented.
- The role of apoptosis in Cd toxicity is not well understood.
Purpose of the Study:
- To investigate the occurrence and characteristics of apoptosis in acute cadmium hepatotoxicity.
- To determine the relationship between apoptosis, necrosis, and regeneration in Cd-induced liver injury.
Main Methods:
- Mice were injected with varying doses of Cd (5-60 mumol/kg).
- Liver tissues were analyzed histopathologically at different time points (1.5-48 h).
- Apoptotic and mitotic indices, DNA fragmentation, and liver enzymes (ALT, SDH) were quantified.
Main Results:
- Cd induced a time- and dose-dependent increase in apoptosis, necrosis, and mitotic index.
- Apoptosis peaked at 9-14 h, preceding the peak of necrosis at 14-48 h.
- Peliosis hepatis and compensatory liver regeneration were observed.
Conclusions:
- Apoptosis is a primary mechanism for eliminating damaged cells in acute Cd hepatotoxicity.
- Apoptosis precedes necrosis, highlighting its role in the early stages of Cd-induced liver injury.
- Cd toxicity elicits a complex response involving cell death and regeneration.