Decrease in hepatotoxicity by lead exposure is not explained by its mitogenic response

✍ Scribed by Edward J. Calabrese; Linda A. Baldwin; Denise A. Leonard; Xiao Qiang Zhao

• Publisher: John Wiley and Sons
• Year: 1995
• Tongue: English
• Weight: 401 KB
• Volume: 15
• Category: Article
• ISSN: 0260-437X
• DOI: 10.1002/jat.2550150212

✦ Synopsis

The present research was conducted to evaluate the effect of mitogen pre-exposure on CCI,-induced hepatotoxicity. Male Wistar rats were administered a single i.p. injection of CCI4 (0.3 ml kg-' in corn oil) 48 h following either a single dose of lead nitrate (0.33 mg kg-') or distilled water via i.v. injection. Hepatotoxicity, as measured by serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, was monitored 6, 24, 48, 72 and 120 h after CCI4 exposure. The lead nitrate-pretreated rats displayed markedly lower serum ALT and AST levels at 24, 48 and 72 h than rats pretreated with distilled water. However, treatment with the antimitotic agent colchicine did not alter the lead-induced protection. These findings suggest that the lead-induced protection is not associated with the major mitogenic response of lead, despite its strong temporal association. A critical review of the available toxicological data also argues against the lead protection being a function of its capacity to inhibit cytochrome P-450.