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Abstract
The effects of inhaled methyl iodide (MeI) on clinical pathology parameters, glutathione (GSH) tissue levels, serum thyroid hormone and inorganic iodide concentrations, S-methylcysteine hemoglobin concentrations, and liver UDP-glucuronyltransferase activity were studied in the rat. Male rats were exposed by whole-body inhalation to 0, 25, or 100 ppm MeI, 6 h/day for up to 2 days. Serum cholesterol concentrations (both high-density lipoprotein [HDL] and low-density lipoprotein [LDL] fractions) were increased and triglycerides were decreased at both exposure levels. Serum thyroid-stimulating hormone (TSH) concentrations were increased at 25 and 100 ppm, and serum triiodothyronine (T3) and thyroxine (T4) concentrations were decreased at 100 ppm. There was no change in either reverse triiodothyronine (rT3) or UDP-glucuronyltransferase activity at either exposure level. A dose- and time-dependent reduction in GSH levels in blood, kidney, liver, and nasal tissue was observed, with the greatest reduction in nasal tissue (olfactory and respiratory epithelium). MeI exposure also resulted in a substantial dose- and time-dependent increase in both serum inorganic iodide and red blood cell S-methylcysteine hemoglobin adducts. These results indicate that following inhalation exposure, MeI is rapidly metabolized in blood and tissue of rats, resulting in methylation products and release of inorganic iodide.
Acknowledgements
This work was performed under contract for Arysta LifeScience Corporation, Cary, NC (formerly named Arvesta Corporation). The technical assistance from members of the Haskell Clinical Pathology (D. Hoban, E. Wilkinson), Necropsy (J. Holt, J. Joyce, L. Lewis, C. Lloyd, S. Records), Inhalation (A. DiMatteo, W. Ellis, J. Nogaj), and Investigative Toxicology (R. Manning, R. Mingoia, S. Mazumdar, B. Shertz, S. Snajdr) and Quality Assurance (J. Hamill) groups is greatly appreciated.
Current affiliation for Nancy E. Everds is Amgen, Inc., Seattle, WA, USA. Current affiliation for Raymond A. Kemper is Boehringer Ingelheim Pharmaceuticals, Inc., Ridgefield, CT, USA.
Declaration of interest: This work was performed under contract for Arysta LifeSciences Corporation, Cary, NC (formerly named Arvesta Corporation). The authors alone are responsible for the content and writing of the paper.