Abstract

Environmental exposure to toxic levels of lead (Pb) occurs in a number of industries with potential adverse effects on the reproductive capacity of exposed men. Clinical and animal studies indicate that abnormalities of spermatogenesis result from toxic lead exposure, but eventual histopathologic alterations involved have not been identified. To explore putative abnormalities in the reproductive gonadotropic axis following lead intoxication, experimental animals when exposed to low levels of lead, 65 days old animals were treated with distilled water containing 0, 0 mg (control), 10 mg lead (Pb)/Kg/day and 15 mg lead (Pb)/Kg/day intraperitoneally for 20 days. At the end of treatment, the animals were sacrificed and the blood collected for luteinizing hormone (LH) and testosterone assays. The testis was processed for histological analysis. The results showed a high serum concentration of LH and testosterone in lead-treated animals compared to controls. Histological examination of testis showed deformities in testicular morphology of lead intoxicated animals with gross damage within the somniferous tubules. A strong correlation was established between LH and testosterone suggesting an alteration in the endocrine components of the gonadotropic axis. Histological examination of pituitary gland showed some degenerative changes in endocrine cells of lead group. Changes in LH and testosterone levels suggest that Pb exposure during the critical time of sexual differentiation induces reproductive axis abnormalities in adulthood. In conclusion, lead has a gonadotoxic effect by decreasing LH and testosterone levels and damaging the testis seminiferous tubules. Catalase activity was significantly reduced in the lead group following 65 days of exposure which possibly indicates that lead might had other mechanisms of action, such as increasing oxidative damage.

Highlights

  • Lead is considered as one of the major environmental pollutants

  • Some works suggested a direct toxic action on the hypothalamic-pituitary axis, such as the study of (Stumpf et al, 1980) which mentioned a fall in the number of spermatozoa in the testis; In addition, other studies showed that the toxicity of lead appears primarily on the interstitial cells by the inhibition of enzymes synthesis implied in the steroidogenesis and of the hormonal receivers (Thoreux-Manlay et al, 1995; Wiebe et al, 1983)

  • Elemental analysis The results of Student’s t-test on lead residues in rat brain treated 20 days with 10 mg/kg and 15 mg/kg of lead acetate revealed that the group treated with 15 mg/ kg of lead acetate had significantly higher concentration of lead in their brains than the group treated with 10 mg/kg (p

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Summary

Introduction

Lead is considered as one of the major environmental pollutants. It may have different origins such as contaminated food, unsanitary preservation of food, lead hydrous piping, industrial pollution, road traffic and drinking water (López-Carrillo et al, 1996). Exposure to lead could damage nervous systems by provoking neuropsychological disturbances (Hogstedt et al, 1983), motor and sensory conduction velocities (Seppäläinen et al, 1983), and alter the heme synthesis (Piomelli, 1981). It can induce acute nephrotoxicity (Goyer, 1989), cause disturbances of the reproductive system (Apostoli et al, 1998; Goyer, 1990) and increase blood pressure (Hertz-Picciotto and Croft, 1993; Schwartz, 1995). The present work was aimed to investigate eventual action of lead on the pituitary and testicular components of the gonadotropic axis underlying alterations in reproductive function

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