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Hepatotoxicity of carbon tetrachloride
Last reviewed: 05.07.2025
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Carbon tetrachloride can enter the body accidentally or as a result of suicidal ingestion. It can be in gas form (for example, during dry cleaning or when filling a fire extinguisher) or mixed with drinks.
Liver damage is caused by a toxic metabolite that acts on cytochrome P450-dependent monooxidase located in the smooth endoplasmic reticulum of perivenular hepatocytes. Its action is enhanced by enzyme inducers such as alcohol and barbiturates and is attenuated by protein starvation, which reduces the activity of drug-metabolizing enzymes.
[ Morphological changes
In hepatocytes of zone 3, hydropic degeneration is revealed in the form of transparent cytoplasm and pyknotic nucleus. Fatty degeneration can be expressed to varying degrees - from single fat drops to diffuse involvement of hepatocytes. Minor infiltration of portal zones by polymorphonuclear leukocytes is noted. Fibrosis is not typical. As recovery proceeds, the morphological picture in the liver returns to normal.
Symptoms
Poisoning is characterized by vomiting, abdominal pain, and diarrhea. Jaundice develops within 2 days. Liver enlargement and tenderness may be observed. Spontaneous bleeding is possible due to severe hypoprothrombinemia. Serum transaminase activity is significantly increased; serum albumin levels are reduced.
In severe cases, acute renal failure comes to the fore. Acute hemorrhagic gastritis is expressed. Due to the fact that carbon tetrachloride is an anesthetic, increasing drowsiness is observed.
Substances similar in structure to carbon tetrachloride
Teenagers who sniff glue containing toluene or household vapors containing trichloroethylene may develop jaundice with liver necrosis and renal failure.
A picture similar to carbon tetrachloride poisoning develops with industrial poisoning with the solvent 1,1,1-trichloroethane.
Benzene derivatives - trinitrotoluene, dinitrophenol and toluene - mainly affect the bone marrow, causing its aplasia. Acute liver damage is possible, but chronic changes are rare.
Contact with industrial organic solvents may result in elevated transaminase levels. Short-term contact (less than 3 months) with the solvent dimethylformamide results in gastrointestinal disturbances, significant increases in transaminase levels, focal hepatocellular necrosis, and microvascular obesity. With longer-term contact (more than 1 year), clinical manifestations are minimal, and transaminase levels are moderately elevated. Liver biopsy reveals microvascular obesity and proliferation of the smooth endoplasmic reticulum.
Electron microscopy of biopsies reveals PAS-positive inclusions and pathological changes in mitochondria.
Occupational exposure to 2-nitropropane can be fatal.
It is possible that not all cases of occupational liver injury are detected. The prognostic significance of long-term occupational exposure to toxic substances is unknown.
Treatment
During preventive examination of workers in contact with carbon tetrachloride, attention should be paid to the size and soreness of the liver, the level of urobilinogen in the urine should be determined, as well as the activity of serum transaminases and GGT.
In acute poisoning, high-calorie, carbohydrate-rich food is prescribed; in cases of acute liver and kidney failure, appropriate treatment is administered, including hemodialysis. Early administration of acetylcysteine can minimize liver and kidney damage.
Forecast
In the acute stage, the cause of death is renal failure. If the victim does not die in the acute stage, then late complications from the liver do not develop. Experiments on rats have shown that repeated intoxications lead to cirrhosis. In humans, such consequences are not observed; with prolonged contact, hepatocytes can even become more resistant to this intoxication. Carbon tetrachloride is not an etiological factor in liver cirrhosis in humans.