Lead, cadmium, endotoxin interaction: Effect on mortality and hepatic function
| Autor: | N. R. Di Luzio, E.A. Marconi, J.A. Cook |
|---|---|
| Rok vydání: | 1974 |
| Předmět: |
Blood Glucose
Male medicine.medical_specialty Time Factors chemistry.chemical_element Acetates Toxicology Methylprednisolone Sulfobromophthalein Transaminase Iodine Radioisotopes chemistry.chemical_compound Liver Function Tests Internal medicine medicine Animals Aspartate Aminotransferases Mononuclear Phagocyte System Cadmium acetate Pharmacology Cadmium Kupffer cell Alanine Transaminase Drug Synergism Mononuclear phagocyte system Rats Endotoxins medicine.anatomical_structure Endocrinology Lead Liver Salmonella enteritidis chemistry Lead acetate Immunology Colorimetry Liver function medicine.drug |
| Zdroj: | Toxicology and Applied Pharmacology. 28:292-302 |
| ISSN: | 0041-008X |
| DOI: | 10.1016/0041-008x(74)90016-7 |
| Popis: | Although iv administration of certain heavy metals, particularly lead, markedly enhances the sensitivity of animals to bacterial endotoxins, the endotoxin-sensitizing potency of the heavy metal cadmium has not been previously investigated. Endotoxin sensitivity and liver function were evaluated comparatively in rats receiving equimolar doses of either lead or cadmium acetate. Additionally, methylprednisolone, which prevents lethality following lead-endotoxin interaction, was administered to cadmium-endotoxin-treated rats. Rats receiving iv cadmium acetate or lead acetate demonstrated enhanced responsiveness to Salmonella enteriditis endotoxin as denoted by increased mortality, impaired sulfobromophthalein (BSP) removal, hypoglycemia, and elevated activity of plasma glutamic-oxaloacetic transaminase (GOT) and glutamic-pyruvic transaminase (GPT). The administration of cadmium acetate alone produced a moderate degree of hepatic dysfunction which was not observed in the lead-treated group. Mortality as well as alterations of blood glucose concentrations and plasma activity of GOT and GPT was greater following combined treatment with cadmium and endotoxin than lead and endotoxin. Animals receiving methylprednisolone were refractory to lead-endotoxin-induced lethality and displayed reduced alterations of plasma BSP removal, plasma glucose, and enzyme activity. However, methylprednisolone did not alleviate the detrimental effect of combined cadmium and endotoxin treatment. Cadmium acetate administration increased intravascular clearance and enhanced Kupffer cell localization of the reticuloendothelial test lipid emulsion. In contrast, clearance rates and hepatic localization of the labeled emulsion were depressed following lead acetate administration. These divergent findings indicate that endotoxin sensitivity induced by lead or cadmium cannot be attributed to phagocytic alterations. Our composite study suggests that hepatic parenchymal cell dysfunction is one facet of the pathophysiology manifested by cadmium or lead interaction with endotoxin. |
| Databáze: | OpenAIRE |
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