Mechanistic study on liver tumor promoting effects of piperonyl butoxide in rats
| Autor: | Takayoshi Imazawa, Hiroshi Onodera, Kazuo Yasuhara, Seiichi Ito, Michihito Takahashi, Kunitoshi Mitsumori, Hideaki Okamiya |
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| Rok vydání: | 1998 |
| Předmět: |
Male
medicine.medical_specialty Piperonyl butoxide Necrosis Liver tumor Piperonyl Butoxide Health Toxicology and Mutagenesis Toxicology Connexins Eating chemistry.chemical_compound Liver Neoplasms Experimental Internal medicine medicine Animals Carcinogen Cell growth Immunochemistry Body Weight Organ Size General Medicine medicine.disease Rats Inbred F344 Rats Specific Pathogen-Free Organisms Intercellular Junctions Endocrinology medicine.anatomical_structure Liver chemistry Phenobarbital Hepatocyte Cytochrome P-450 CYP2B1 Toxicity Carcinogens medicine.symptom Cell Division medicine.drug |
| Zdroj: | Archives of Toxicology. 72:744-750 |
| ISSN: | 1432-0738 0340-5761 |
| DOI: | 10.1007/s002040050569 |
| Popis: | Piperonyl butoxide, alpha-[2-(2-butoxyethoxy)ethoxy]-4,5-methylenedioxy-2-propyltol uene, is a widely used pesticide-synergist. Recently, results were reported indicating that piperonyl butoxide is a hepatocarcinogen in rat. Since the underlying mechanism was not elucidated, we examined the effects on rat liver cells in detail. For this purpose male F344 rats were administered piperonyl butoxide mixed in the diet at concentrations of 0 (negative control), 0.05, 0.2 or 2% for 2 days, 1, 2, and 4 weeks. As a positive control, phenobarbital was administered to rats for up to 4 weeks as a 0.1% solution in the drinking water. Increased liver weight, centrilobular hepatocellular hypertrophy due to increased smooth endoplasmic reticulum, decreased numbers and areas of connexin 32-positive spots per hepatocyte, and increased cell proliferation were observed in rats treated with 0.2 and 2% piperonyl butoxide. Similar results were obtained for 0.1% phenobarbital treated rats. Hepatocellular necrosis suggestive of hepatotoxicity was also observed in the 2% piperonyl butoxide group. These results indicate that the promoting mechanism of piperonyl butoxide in hepatocarcinogenesis is similar to that of phenobarbital, involving an ability to induce CYP isoenzymes and inhibit gap junctional intercellular communication. In addition, increased cell proliferation following hepatocellular necrosis may also play a role at high doses. |
| Databáze: | OpenAIRE |
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