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Effect of modeccin on rat liver ribosomes in vivo
Abstract:
1. Rat liver microsomes isolated at 6 and 12 h of poisoning with 3 x LD50 (0.3 microgram/100 g body wt.) of modeccin, the toxin of Adenia digitata, have a decreased capacity of protein synthesis in vitro. 2. A similar decrease of protein synthesis is observed with polysomes at 6 h of poisoning. Experiments with recombined ribosomal subunits demonstrate that this is due to inactivation of the 60 S ribosomal subunit. 3. At 6 h of poisoning there is a marked vesiculation and degranulation of the hepatocyte rough endoplasmic reticulum, which is completely fragmented at 24 h of poisoning. Hepatocyte mitochondria are swollen at 6 h and shrunk at 24 h of poisoning. 4. It is concluded that modeccin penetrates inside hepatocytes in vivo, and damages ribosomes in the same manner as it does in vitro. However, mitochondrial damage indicates that ribosomes may not be the only target of modeccin in vivo.
Insights
Modeccin toxin from Adenia digitata inhibits protein synthesis in rat liver cells by damaging the 60S ribosomal subunit. Further research is needed as mitochondrial damage suggests other cellular targets may also be affected.
Area of Science:
- Toxicology
- Molecular Biology
- Cell Biology
Background:
- Modeccin is a toxin isolated from Adenia digitata.
- Toxins can disrupt cellular functions, including protein synthesis.
Purpose of the Study:
- To investigate the effects of modeccin on protein synthesis in rat liver cells.
- To identify the specific cellular targets of modeccin.
Main Methods:
- In vitro protein synthesis assays using rat liver microsomes and polysomes.
- Recombination experiments with ribosomal subunits.
- Electron microscopy of hepatocytes.
Main Results:
- Modeccin significantly decreased protein synthesis capacity in rat liver microsomes and polysomes.
- Inactivation of the 60S ribosomal subunit was identified as the cause of reduced protein synthesis.
- Hepatocytes showed damage to the rough endoplasmic reticulum and mitochondria.
Conclusions:
- Modeccin enters hepatocytes and inhibits protein synthesis by damaging ribosomes.
- Mitochondrial damage suggests that ribosomes may not be the sole in vivo target of modeccin.