|
|
||||||||
1 From the Biological Laboratories, Harvard University
In the catfish, with prolonged exposure to a solution of lead acetate, definite evidence of absorption of lead was obtained. The surface mucus did not constitute an efficient barrier to the entrance of the metal as Carpenter (1927, 1930) found in more acute experiments with fishes in which a lethal reaction was frequently obtained.
The degree of destruction of the erythrocytes was used as a measure of the rate of the absorption of lead. Following the early evidences of injury to the blood cells, a mild regenerative response occurred, but eventually a pronounced secondary anemia was produced. Little phagocytosis of dead cells occurred in the peripheral circulation, but a progressive storage of the pigment derived from dead red blood cells was found in the interstitial tissues of the liver, spleen, and mesonephros. The hepatic cells also became crowded with pigment granules. No storage was observed in the heart. The pigment was accumulated chiefly in macrophages of local origin which, after ingesting erythrocytes, desquamated and migrated into the connective tissues.
Monocytes and eosinophiles were increased slightly in number in the blood stream, but the most striking change occurred in the numbers of atypical thrombocytes, and spindle cells which may belong to the thrombocytic series.
The endothelium of the heart showed marked proliferative activity. In some regions there was localized differentiation of erythrocytes. In other regions the atypical elongated cells, just referred to, were formed in large radiating clusters on the surface of the ventricular trabeculae. No explanation of the latter response to lead poisoning can be given.
This article has been cited by other articles:
![]() |
J. C. Wolf and M. J. Wolfe A Brief Overview of Nonneoplastic Hepatic Toxicity in Fish Toxicol Pathol, January 1, 2005; 33(1): 75 - 85. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |