Effects of Dietary Ascorbic Acid on Chronic Lead Toxicity to Young Rainbow Trout (Salmo gairdneri)

1980 ◽  
Vol 37 (2) ◽  
pp. 170-176 ◽  
Author(s):  
P. V. Hodson ◽  
J. W. Hilton ◽  
B. R. Blunt ◽  
S. J. Slinger
Keyword(s):  
Ascorbic Acid ◽  
Rainbow Trout ◽  
Lead Toxicity ◽  
Blood Lead ◽  
Salmo Gairdneri ◽  
Spinal Curvatures ◽  
Ascorbic Acid Deficiency ◽  
Vitamin Deficiencies ◽  
Amino Levulinic Acid ◽  
Acid Deficiency

Newly hatched rainbow trout (Salmo gairdneri) exposed to waterborne lead and receiving diets deficient in, or supplemented with, ascorbic acid, developed classical symptoms of lead toxicity and ascorbic acid deficiency. Those exposed to lead showed elevated blood lead concentrations, inhibition of erythrocyte δ-amino levulinic acid dehydratase, darkening of the tail regions and spinal curvatures. Those receiving ascorbate deficient diets showed depletion of carcass, liver, kidney, and brain ascorbic acid concentrations plus spinal curvatures. Fish subjected to both treatments simultaneously showed no evidence of an enhancement of ascorbate deficiency symptoms by exposure to lead or enhancement or reduction of lead toxicity symptoms by ascorbate deficient or supplemented diets, respectively. These results demonstrate that, although aspects of lead toxicity in fish resemble ascorbic acid deficiency, there is no metabolic interaction between the two factors.Key words: pollutants, toxicity, interaction, lead, vitamin deficiencies, Salmonidae, rainbow trout

pH-Induced Changes in Blood Lead of Lead-Exposed Rainbow Trout (Salmo gairdneri)

1978 ◽  
Vol 35 (4) ◽  
pp. 437-445 ◽  
Author(s):  
Peter V. Hodson ◽  
Beverly R. Blunt ◽  
Douglas J. Spry
Keyword(s):  
Rainbow Trout ◽  
Lead Toxicity ◽  
Blood Lead ◽  
Salmo Gairdneri ◽  
Lead Uptake ◽  
Exposure System ◽  
Test Water ◽  
Induced Changes ◽  
Inorganic Constituents ◽  
Uptake And Release

Blood of juvenile rainbow trout (Salmo gairdneri) exposed to lead in water showed increasing lead concentrations as pH of the test water decreased from 10.0 to 6.0. A decrease in pH by 1.0 unit from any reference pH resulted in an increase of blood lead by a factor of 2.1. Since sublethal lead toxicity is related to uptake, these results suggest that toxicity increases as pH decreases. Control experiments indicated that reactions of lead with inorganic constituents of the test water were complete within 3 h and that blood lead was at equilibrium with water lead within 48 h. Therefore, at the time of blood sampling in the pH experiment, both lead complexation processes in the exposure system, plus lead uptake and release from the blood, were at equilibrium. Key words: pH, lead, toxicity, fish, Salmo, blood, equilibrium.

Multiple Vitamin Deficiencies in Association With Chronic Anticonvulsant Therapy

PEDIATRICS ◽  
1977 ◽  
Vol 60 (5) ◽  
pp. 767-767
Author(s):  
Gordon L. Klein ◽  
James B. Florey ◽  
Vernon L. Goller ◽  
Ricci J. Larese ◽  
Quentin L. Van Meter
Keyword(s):  
Ascorbic Acid ◽  
Clinical Evidence ◽  
Anticonvulsant Therapy ◽  
Vitamin Supplementation ◽  
Black Girl ◽  
Ascorbic Acid Deficiency ◽  
Vitamin Deficiencies ◽  
Full Diet ◽  
Acid Deficiency

Tolman et al. (Pediatrics 56:45, July 1975) and Crosley et al. (Pediatrics 56:52, July 1975) described rickets and osteomalacia complicating chronic anticonvulsant therapy. We recently cared for a 28-month-old black girl who not only developed the physical and roentgenographic stigmata of rickets while receiving long-term anticonvulsants, but who also demonstrated clinical evidence of cardiac beriberi and subclinical ascorbic acid deficiency. The patient was receiving acceptable doses of phenobarbital, Dilantin, and Mysoline for infantile myoclonic seizures, was allegedly fed a full diet in the nursing home in which she was cared for, but did not receive vitamin supplementation.

Evaluation of Erythrocyte δ-amino Levulinic Acid Dehydratase Activity as a Short-Term Indicator in Fish of a Harmful Exposure to Lead

1977 ◽  
Vol 34 (4) ◽  
pp. 501-508 ◽  
Author(s):  
Peter V. Hodson ◽  
Beverley R. Blunt ◽  
Douglas J. Spry ◽  
Keith Austen
Keyword(s):  
Rainbow Trout ◽  
Brook Trout ◽  
Levulinic Acid ◽  
Blood Lead ◽  
Salmo Gairdneri ◽  
Lepomis Gibbosus ◽  
Experimental Conditions ◽  
Goldfish Carassius Auratus ◽  
Acid Dehydratase ◽  
Amino Levulinic Acid

The activity of erythrocyte δ-amino levulinic acid dehydratase (ALA-D) of fish is easily measured under a variety of experimental conditions. Exposure of rainbow trout (Salmo gairdneri), brook trout (Salvelinus fontinalis), goldfish (Carassius auratus), and pumpkinseeds (Lepomis gibbosus) to lead consistently inhibited ALA-D within 2 wks at concentrations as low as 10, 90, 470, and 90 μg/ℓ, respectively. In rainbow and brook trout these concentrations were closely related to the published minimum effective concentrations causing sublethal harm. There was a significant linear relationship between ALA-D activity and log of blood lead concentration, between ALA-D activity and log of lead in water, and between blood lead and lead in water. Near lethal exposures to cadmium, copper, zinc, and mercury did not significantly inhibit ALA-D activity. Recovery of ALA-D activity of rainbow trout after transfer from 120 μg/ℓ lead to clean water occurred in 8 wk. This enzyme provides fast, consistent, specific, and sensitive estimates of lead concentrations causing sublethal harm to fish and may help to relate sources of lead to degree of exposure of fish populations in the field. Key words: lead, sublethal toxicity, fish, indicator enzyme, δ-amino levulinic acid dehydratase

EXPERIMENTAL ATHEROSCLEROSIS WITH ASCORBIC ACID DEFICIENCY

1971 ◽  
Vol 35 (12) ◽  
pp. 1559-1565 ◽  
Author(s):  
TAKAO FUJITANI ◽  
KOTA OKADO ◽  
KATSUJI SENDA ◽  
MUNEAKI SUGIMURA ◽  
MOTOAKI KISHIKAWA
Keyword(s):  
Ascorbic Acid ◽  
Experimental Atherosclerosis ◽  
Ascorbic Acid Deficiency ◽  
Acid Deficiency

Ascorbic Acid Deficiency —

1981 ◽  
Vol 5 (6) ◽  
pp. 531-532 ◽  
Author(s):  
R.E. Hodges ◽  
J.E. Canham ◽  
J.L. Smith
Keyword(s):  
Ascorbic Acid ◽  
Ascorbic Acid Deficiency ◽  
Acid Deficiency

Effect of ascorbic acid deficiency on primary and reparative dentinogenesis in non-ascorbate-synthesizing ods rats

1997 ◽  
Vol 42 (10-11) ◽  
pp. 695-704 ◽  
Author(s):  
Motonari Ogawara ◽  
Kazuhiro Aoki ◽  
Takashi Okiji ◽  
Hideaki Suda
Keyword(s):  
Ascorbic Acid ◽  
Ascorbic Acid Deficiency ◽  
Acid Deficiency
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