Date of Award

12-1994

Document Type

Thesis

Degree Name

Master of Science (MS)

Department

Biology

First Advisor

Amna Hamad AI Dhaheri

Second Advisor

Mohamed A. Fahim, Ph.D.

Third Advisor

Nawal Abdel-Hey Ahmed, Ph.D.

Abstract

Lead is one of many heavy metal ions that can effectively compete for the binding sites of calcium, block the calcium channels and disturb the ion exchange. As a result, lead would be expected to affect the calcium-mediated cell functions. Muscle contraction and platelet aggregation are two important functions in which Ca2+ plays a major role and ultimately are affected by lead. Experiments were carried out to investigate the effect of lead on mouse flexor muscle contraction and on photochemically-induced platelet aggregation in pial microcirculation. A study of an acute exposure (1, 5, 10 and 25 µM) and a chronic exposure to lead of 0.1 mg/kg (low dose) and 1 mg/kg bodyweight (high dose), injected subcutaneously for 7 days were carried out on flexor muscles. The acute lead exposure reduced specific twitch tension of the muscle in a dose dependent fashion, accelerated muscle fatigue and altered the frequency-tension relationship. Muscle fibers of chronically treated mice when examined by an electron-microscope, and as compared to control, showed ultrastructural changes in both intramuscular myelinated axons and neuromuscular junctions. Effect of chronic lead treatment on phtochemically-induced platelet aggregation in pial microcirculation was also investigated. Findings showed a significant decrement in the time needed to form the first observable platelet aggregate only in arterioles in both the low and high lead doses. This result suggests an enhanced susceptibility to thrombosis in these microvessels, which would ultimately reduce blood supply to the tissue involved. Since Ca2+ is an essential ingredient in these two biological functions, interference of lead with Ca2+ binding sites and/or ionic exchange could form a possible explanation for these findings.

Included in

Biology Commons

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