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Light and electron microscopic observations of the acute sublethal hepatotoxic effects of Mirex in the rat
Abstract:
The fire-ant poison, Mirex, was administered via stomach tube (dosage 200 mg/kg) to 50 adult Mai-Wistar male rats and the resultant histopathologic lesions produced in their livers after six days post-intubation are described. Light (LM) and electron microscopic (EM) technques revealed cellular and subcellular alterations in response to this sublethal dosage. Pathologic lipid accumulations occurred in Mirex-exposed rats and this fat appeared in a distinctive periportal zonation pattern. Additional lesions were detected in centrolobular zones with the EM and included severe glycogen depletion, altered regularity in the architecture of rough or granular endoplasmic reticulum (GER), dilated GER cisternae, free ribosomes, and proliferation of smooth endoplasmic reticulum. Periportal hepatocytes exhibited apparent reduction in numbers of cytoplasmic organelles and development of many, large lipid-containing vacuoles. Myelin figures were sometimes associated with developing lipid (liposomes), suggesting a contribution of myelin membranes to the developing lipid droplets or vice versa. Biochemical studies revealed that glycogen levels dropped markedly, lipid content greatly increased, and protein/DNA and RNA/DNA values decreased.
Insights
Mirex, a fire-ant poison, caused significant liver damage in rats, including fat accumulation and altered cellular structures. This study details the histopathologic and biochemical changes following Mirex exposure.
Area of Science:
- Toxicology
- Hepatopathology
- Cell Biology
Background:
- Mirex is a persistent organochlorine insecticide used to control fire ants.
- Organochlorine pesticides can accumulate in fatty tissues and exert toxic effects on various organs, including the liver.
- Understanding the specific hepatic effects of Mirex is crucial for assessing its toxicological risks.
Purpose of the Study:
- To investigate the histopathologic and subcellular alterations in rat livers following Mirex administration.
- To characterize the pattern and extent of liver damage induced by a sublethal dose of Mirex.
- To correlate observed cellular changes with biochemical alterations in liver tissue.
Main Methods:
- Administration of Mirex (200 mg/kg) via stomach tube to adult male Mai-Wistar rats (n=50).
- Histopathological examination of liver tissues using light microscopy (LM) and electron microscopy (EM) six days post-intubation.
- Biochemical analysis of liver tissue for glycogen, lipid, protein, and nucleic acid content.
Main Results:
- Mirex exposure led to significant lipid accumulation in hepatocytes, predominantly in a periportal zonation pattern.
- Electron microscopy revealed glycogen depletion, disrupted granular endoplasmic reticulum (GER), and proliferation of smooth endoplasmic reticulum in centrolobular zones.
- Periportal hepatocytes showed reduced organelle numbers and numerous lipid-filled vacuoles; myelin figures were associated with lipid droplet formation.
- Biochemical assays confirmed marked glycogen depletion, a substantial increase in total lipid content, and decreased protein/DNA and RNA/DNA ratios.
Conclusions:
- Sublethal Mirex exposure induces distinct histopathologic lesions in rat livers, characterized by zonal lipidosis and significant alterations in endoplasmic reticulum and glycogen stores.
- The observed cellular and subcellular changes suggest Mirex interferes with lipid metabolism and cellular structure maintenance.
- Biochemical data support the histopathological findings, indicating Mirex disrupts energy storage and cellular macromolecule synthesis in the liver.