Volume 11, Issue 2, November – December 2011; Article-018 ISSN 0976 – 044X International Journal of Pharmaceutical Sciences Review and Research Page 91 Available online at www.globalresearchonline.net Sachdev Yadav, Dr. Veena Sharma Assistant Professor, Department of Pharmacy, Banasthali University, Rajasthan, India. Associate Professor, Department of Biosciences and Biotechnology, Banasthali University, Rajasthan, India. * Corresponding author’s E-mail: sachdev_y@yahoo.com Accepted on: 28-08-2011; Finalized on: 28-11-2011. ABSTRACT It has been known since ancient times that lead is virtually toxic to every organ of body including central nervous system where it may manifest as encephalopathy and hyposmia yet the exact mechanism of these clinical manifestations remains inconclusive. The present study was aimed to see the microscopic changes in the olfactory bulb of mice induced by oral administration of a lead compound in adult albino mice. A total number of 20 adult albino mice of either sex were included in the present study consisting of equal numbers in both control and experimental groups. Experimental group received 4.5% and 5% lead nitrate and lead acetate trihydrate orally for a period of 3 weeks then animals of both groups were euthanized with overdose of general anaesthesia and perfused with 10% formalin. Olfactory bulbs were dissected out and processed for paraffin embedding. Sections of 10μ thick were stained with H&E and observed under light microscope. On gross examination brains from the experimental group revealed generalized edema and petechial haemorrhages. Histopathology of the olfactory bulbs revealed edema and congestion with vacuoles of variable sizes almost throughout. Distortion of glomeruli, clumping of periglomerular cells and increasing number of pyknotic cells were also noticed. It was concluded that lead has toxic effects on the central nervous system including olfactory bulb in the form of edema, microscopic hemorrhages and neuronal loss which may explain the clinical manifestations of lead toxicity. Keywords: Albino mice, Olfactory bulb, Lead nitrate and lead acetate trihydrate, Hyposmia. INTRODUCTION It has been known since ancient times that lead may cause poisoning in man 1 . Exposure of lead can take place either through inhalation of dust, fumes, vapors or ingestion of contaminated foods or drinks. Because of its cumulative property it is capable of exerting toxic effects at any level of exposure. Toxic effect of lead on the body is known as Plumbism and it is now well recognized that inorganic lead produces not only clinically defined encephalopathies and neuropathies, but also various behavioral changes indicative of cerebral dysfunction. However, only within the past fifty years attention has been called to its effects in children 2, 3 in whom toxicity can easily be overlooked until clinically recognizable encephalopathy occurs. The brain is exceptionally sensitive to the effects of lead poisoning 4 , and it is the young-from birth to about 7 years of age who show the most serious brain damage following lead poisoning. The clinical manifestations of lead poisoning are well defined and include headache, incoordination, tremor, twitching, convulsion, paralysis, coma and death 5 . In the brain, cerebellum was found to be most severely affected 6 . Significant decrease in spine density 7 and reduction in the maximum width of the hippocampus 8 have also been reported. Bilaterally symmetrical spongiform changes in the roof nuclei of cerebellum 9 was also reported in dogs exposed to orally fed lead while bilaterally symmetrical areas of vacuole formation were observed at the tips of cortical gyri 10 . Other heavy metals like Cadmium dust induced anosmia 11 and in another study it was reported that inhalation of cadmium affected olfactory bulb and contributed to olfactory dysfunction 12 . Zinc gluconate trihydrate induced cellular and tissue damages to olfactory neuroepithelium and to mitral cells in rat olfactory bulb 13 . Exposure to high levels of mercury (a heavy metal) has also been thought to cause olfactory loss 14 . The present study was aimed to see the effect of lead on the histology of the olfactory bulb which may explain the olfactory dysfunction in the individuals exposed to lead. M ATERIALS AND M ETHODS A total number of 20 adult albino mice (10 male & 10 female) weighing 30g (±10g) were used in the present study. Mice with equal number of either sex 4 (2 male and 2 female) were treated with 4.5% and 5% lead nitrate and lead acetate trihydrate respectively, while the other 4 (2 male and 2 female) served as control did not receive any active compound. The concentration of lead nitrate and lead acetate trihydrate was ascertained after a careful trial in order to find maximum survival of 15 to 20 days. After this period, mice were anaesthetized with ether and perfused with buffered 10% formalin. Both olfactory bulbs were dissected out from superior aspect and separated from the brain. Olfactory bulbs were cut transversely into two parts and processed for paraffin embedding. From each blocks 10μ thick sections were cut with rotary microtome. Haematoxylin and Eosin stained sections were used for light microscopic observations. Observations On histological examination of olfactory bulb of treated group, it was observed that as compared to control (Fig. 1 A, B, C and D) there was generalized edema and congestion in almost all layers of olfactory bulb. HISTOPATHOLOGICAL EVALUATION OF LEAD INDUCED HYPOSM IA IN ADULT ALBINO M ICE Research Article