Folic Acid Anemia in Coho Salmon

1969 ◽  
Vol 26 (1) ◽  
pp. 111-114 ◽  
Author(s):  
Charlie E. Smith ◽  
John E. Halver
Keyword(s):  
Folic Acid ◽  
Coho Salmon ◽  
Macrocytic Anemia ◽  
Folic Acid Deficiency ◽  
Blood Cell Count ◽  
Deficient Diet ◽  
Blood Smears ◽  
Acid Deficiency ◽  
Red Blood Cell Count ◽  
Peripheral Blood Smears

Juvenile coho salmon (Oncorhynchus kisutch) fed a folic acid-deficient diet and sampled at 6, 9, 12, and 14 weeks developed macrocytic anemia. The anemia, first observed at 6 weeks, was characterized by a significant reduction in red blood cell count as well as macrocytosis and poikilocytosis of erythrocytes. The abnormally shaped erythrocytes observed in peripheral blood smears may be an important aid in the identification of folic acid deficiency in coho salmon. Gross manifestations of the deficiency were extremely pale gills; exophthalmia, often accompanied by ascites fluid; dark coloration; and reduction in growth. Fish recovered after 8 weeks on a diet adequate in folic acid and exhibited a normal blood picture.

Hematological Changes in Coho Salmon Fed a Folic Acid Deficient Diet

1968 ◽  
Vol 25 (1) ◽  
pp. 151-156 ◽  
Author(s):  
Charlie E. Smith
Keyword(s):  
Folic Acid ◽  
Peripheral Blood ◽  
Coho Salmon ◽  
Macrocytic Anemia ◽  
Oncorhynchus Kisutch ◽  
Folic Acid Deficiency ◽  
Deficient Diet ◽  
Acid Deficiency ◽  
Hematological Changes

Coho salmon (Oncorhynchus kisutch) fed a diet deficient in folic acid for 24 weeks developed megaloblastic, normochromic macrocytic anemia. The anemia was further characterized by the presence of poikilocytic erythrocytes which were observed in stained preparations of peripheral blood. These abnormally shaped cells appear to be an important aid in the identification of folic acid deficiency. The anemia disappeared when the deficient fish were fed a recovery diet containing folic acid for 8 weeks.

scholarly journals Folates: Key Nutrients to Remember

2017 ◽  
Vol 9 (2) ◽  
pp. 75
Author(s):  
Gourchala Freha ◽  
Mihoub Fatma ◽  
Henchiri Cherifa
Keyword(s):  
Folic Acid ◽  
Macrocytic Anemia ◽  
Folic Acid Supplementation ◽  
Intestinal Lumen ◽  
Folic Acid Deficiency ◽  
Hydrogen Atoms ◽  
Rapid Multiplication ◽  
Vitamin B9 ◽  
Acid Deficiency ◽  
Pteroylglutamic Acid

Folic acid or vitamin B9 or pteroylglutamic acid, is a relatively simple molecule with two characteristics; firstly, it must be reduced by 2 or 4 hydrogen atoms to be metabolically active which makes it sensitive to oxidation and must be protected by ascorbic acid, secondly it may include in addition to the constituent residues of the molecule, 1-7 glutamate residue at one of its ends. These polyglutamate forms that make up the largest share of food folate, must be deconjugated by a specific enzyme present in the intestinal lumen before being absorbed in the jejunum. It is in the methylated form after passing through the enterocyte it is transported in the blood, excreted in bile and reabsorbed. It must be demethylated to integrate folic cell cycle and methyl transfer, that allows the synthesis of methionine (only possible in the presence of vitamin B12), purine, serine and especially thymidylic acid, constitutive DNA. As a methyl donor that plays a fundamental role in cerebral and nervous metabolism. Folates are involved in cell division thus; any folic acid deficiency causes a slowdown in rapid multiplication systems which may lead to red blood cell disorders (macrocytic anemia), immunity, and neural tube defects, in addition to physiological disorders (cardiovascular, cancer ...). Folic acid supplementation appears to allow the correction of these disorders.

FOLIC-ACID DEFICIENCY IN PREGNANCY

The Lancet ◽  
1959 ◽  
Vol 274 (7110) ◽  
pp. 1033-1034 ◽  
Author(s):  
H.H. Francis ◽  
J.S. Scott
Keyword(s):  
Folic Acid ◽  
Folic Acid Deficiency ◽  
Acid Deficiency ◽  
In Pregnancy
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