Lead exposure alters the drug metabolic activity and the homeostasis of essential metal ions in the lenticular system of the rat

Abstract

Potential lead exposure to the eyes as a result of the use of traditional cosmetic Kohl in Asia, Africa and the Middle East has been a subject of recent debate to the scientific community. In continuation of our earlier work we therefore examine in the present study, the drug metabolic activity and the homeostasis of essential metal ions in the lenticular system of adult rats exposed to long term low level lead (lead acetate 0.1% w/v). The results of our investigation demonstrate that long term low level lead exposure impaired the phase I & phase II metabolic activity of the lenticular system when assessed by aminopyrine demethylase, benzo[a]pyrene hydroxylase, aniline hydroxylase and UDP glucuronyl transferase (UDPGT), glutathione S-transferase (GST), respectively. A more pronounced decrease (55%) in GST was noticed compared to UDPGT, aminopyrene demethylase, benzo[a]-pyrene hydroxylase and aniline hydroxylase (20–30%). Increased lead concentration in the lenticular system of the rats as monitored by atomic absorption spectroscopy resulted in a significant decrease (15–35%) in the levels of Ca, Cu, Zn and Fe, along with a progressive loss in body weight. Respective increase in blood lead level was also monitored parallel to increase in lenticular lead concentration at different time points in lead treated rats. The present investigation, therefore, demonstrates that long term low level lead exposure to rats results in a profound impairment in the homeostasis of essential metal ions, lenticular drug metabolizing enzymatic activity and significant loss in body weight when compared to untreated control rats. Whether such a decrease in these functions reflects an inhibition of protein synthesis at transcriptional/post transcriptional levels or gene regulation at molecular level remains to be established.