Morphological and morphometrical changes in chloride cells of the gills of Pimephales promelas after chronic exposure to acid water

1984 ◽  
Vol 236 (1) ◽  
pp. 121-128 ◽  
Author(s):  
RichardL. Leino ◽  
J.Howard McCormick
Author(s):  
Richard L. Leino ◽  
Jon G. Anderson ◽  
J. Howard McCormick

Groups of 12 fathead minnows were exposed for 129 days to Lake Superior water acidified (pH 5.0, 5.5, 6.0 or 6.5) with reagent grade H2SO4 by means of a multichannel toxicant system for flow-through bioassays. Untreated water (pH 7.5) had the following properties: hardness 45.3 ± 0.3 (95% confidence interval) mg/1 as CaCO3; alkalinity 42.6 ± 0.2 mg/1; Cl- 0.03 meq/1; Na+ 0.05 meq/1; K+ 0.01 meq/1; Ca2+ 0.68 meq/1; Mg2+ 0.26 meq/1; dissolved O2 5.8 ± 0.3 mg/1; free CO2 3.2 ± 0.4 mg/1; T= 24.3 ± 0.1°C. The 1st, 2nd and 3rd gills were subsequently processed for LM (methacrylate), TEM and SEM respectively.Three changes involving chloride cells were correlated with increasing acidity: 1) the appearance of apical pits (figs. 2,5 as compared to figs. 1, 3,4) in chloride cells (about 22% of the chloride cells had pits at pH 5.0); 2) increases in their numbers and 3) increases in the % of these cells in the epithelium of the secondary lamellae.


1990 ◽  
Vol 68 (2) ◽  
pp. 234-244 ◽  
Author(s):  
R. L. Leino ◽  
J. H. McCormick ◽  
K. M. Jensen

Thirty-day-old fathead minnows, Pimephales promelas, were reared at different pH values in softened Lake Superior water enriched with aluminum: pH 7.5–35 μg Al/L, pH 5.5–30 μg Al/L, pH 5.2–35 and 60 μg Al/L, including a background level of 15 μg Al/L, and at pH 7.5, 6.0, 5.5, and 5.2 at background Al levels. Spawning was greatly reduced at pH 6.0, pH 5.5–30 μg Al/L, and pH 5.5 and failed at pH 5.2 with or without added Al. The adult brood stock exhibited abnormalities at low pH, which could have contributed to poor spawning success or energy utilization: (i) thickened respiratory epithelium in the gills, (ii) hyperplasia of primary lamellar epithelium in the gills, (iii) increased number of gill chloride cells, (iv) reduced gill perfusion, (v) immature ovaries and oocyte atresia, (vi) immature and pathologic testes, (vii) abnormal distal tubules and collecting ducts in the kidneys, and (viii) reduced blood osmolality at pH 5.5 and 5.2 when no Al was added. Hatching success and larval survival were reduced when spawning occurred at or below pH 6.0; these larvae often had retarded swim bladder development and yolk absorption and some stages had abnormal gills, kidneys, and liver glycogen reserves. This study further supports the relationship between acidification, histological changes, ionoregulatory disturbances, altered energy metabolism, and recruitment failure.


Author(s):  
J.C.S. Kim ◽  
M.G. Jourden ◽  
E.S. Carlisle

Chronic exposure to nitrogen dioxide in rodents has shown that injury reaches a maximum after 24 hours, and a reparative adaptive phase follows (1). Damage occurring in the terminal bronchioles and proximal portions of the alveolar ducts in rats has been extensively studied by both light and electron microscopy (1).The present study was undertaken to compare the response of lung tissue to intermittent exposure to 10 ppm of nitrogen dioxide gas for 4 hours per week, while the hamsters were on a vitamin A deficient diet. Ultrastructural observations made from lung tissues obtained from non-gas exposed, hypovitaminosis A animals and gas exposed animals fed a regular commercially prepared diet have been compared to elucidate the specific effect of vitamin A on nitrogen dioxide gas exposure. The interaction occurring between vitamin A and nitrogen dioxide gas has not previously been investigated.


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