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Urinary coproporphyrin in lead intoxication: a study in the rabbit
Clinical Science (London, England : 1979)
|November 1, 1983
Summary
Lead exposure in rabbits caused increased coproporphyrin in urine and kidneys. The kidneys play a significant role in excreting excess coproporphyrin, indicating renal origin of this porphyrin.
Area of Science:
- Toxicology
- Biochemistry
- Renal Physiology
Background:
- Lead poisoning is a significant health concern.
- Porphyrin metabolism is often disrupted by lead exposure.
- The role of the kidney in lead-induced porphyrinuria requires further elucidation.
Purpose of the Study:
- To investigate the origin of coproporphyrinuria in lead-intoxicated rabbits.
- To assess the impact of lead acetate on renal porphyrin handling and metabolism.
- To examine the activity of key enzymes in the heme biosynthetic pathway within renal mitochondria.
Main Methods:
- Administration of lead acetate in drinking water to New Zealand White rabbits.
- Measurement of blood lead levels, urine and plasma coproporphyrin, and creatinine clearance.
- Analysis of porphyrin concentrations in renal tissue and assessment of heme biosynthetic enzyme activities (ferrochelatase, coproporphyrinogen oxidase, 5-aminolaevulinate synthase) in renal mitochondria.
Main Results:
- Lead intoxication led to elevated blood lead levels and marked coproporphyrinuria.
- Renal clearance of coproporphyrin significantly increased, while creatinine clearance remained unchanged.
- Elevated levels of lead and various porphyrins were found in renal tissue; enzyme assays revealed decreased coproporphyrinogen oxidase and increased 5-aminolaevulinate synthase activities in lead-intoxicated rabbits.
Conclusions:
- The kidneys are a major source of the excess coproporphyrin excreted during lead intoxication.
- Lead exposure alters renal porphyrin metabolism and excretion pathways.
- Changes in heme biosynthetic enzyme activities within the kidney contribute to the observed porphyrin abnormalities.