Agriculture Reference
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anemia, indistinguishable from that due to folic acid deficiency, ensues. This is part
of the methyl trap hypothesis in which folate is trapped as its 5-methyl derivative
in the DNA cycle. A further consequence of B 12 deficiency is reduced synthesis of
folylpolyglutamates, the active form of folate within cells. Thus, folate deficiency
becomes part and parcel of vitamin B 12 deficiency (Shane and Stokstad 1985). Later,
neurological signs, subacute combined degeneration (SCD) of the spinal cord, occur,
due to interference with the methylation cycle by which methionine converts to
S-adenosyl methionine (SAM), which supplies methyl groups to myelin basic pro-
tein, which insulates nerve cells. Without this, demyelination occurs, leading to
ataxia, paralysis, and eventually death. This also eventually occurs in folic acid defi-
ciency, but much later.
v i t a m i n b 12 s t a t u s
Vitamin B 12 status is currently best estimated as serum vitamin B 12 , which can be
measured using a radioligand-binding assay.
vItAmIn A
The history of our knowledge about the fat-soluble vitamin A was beautifully
described by George Wolf (1996). It goes back to Egyptian papyri written 1 to 2
millennia B.C. Even then, liver was recognized as an effective cure for eye diseases,
used both topically and orally. There have been numerous repeats of those findings
right up to the mid-nineteenth century, when night blindness beset those on board a
ship of the Austrian Navy on a 3-year voyage of discovery. This was again cured by
boiled ox liver. Soon after, Bitot gave his name to the white spots at the conjunctiva-
cornea junction that were associated with night blindness. Mori, in 1904, described
xerophthalmia and keratomalacia in Japanese children. Yet again, liver, and par-
ticularly cod liver oil, was the cure. Eventually, around 1910, research in rats by two
separate groups identified the active fat-soluble factor—“A” (Wolf 1996). This was
isolated and characterized in the 1930s after realizing that the bioactive yellow pig-
ments found in plants, butter fat, and egg yolk could be converted into a colorless
bioactive form in animal liver. The former are now termed provitamin A carote-
noids, while the latter is retinol .
Several decades before, research into the physiology of vision was active, and
by 1881, rod and cone vision were distinguished; it was considered that in night
blindness, the visual purple, which was limited to the peripheral rods used for night
vision, was altered. Most of the advances in knowledge on this subject during the
twentieth century were made by Wald (1968). He showed that the visual purple, or
rhodopsin, was a protein (opsin) combined with retinaldehyde, an active form of
vitamin A. He went on to demonstrate that 11- cis -retinaldehyde is isomerized to all-
trans -retinaldehyde by light (photons), and this reaction triggers a nerve impulse sent
to the brain, which registers it as light.
Thus, the classical signs of vitamin A deficiency are night blindness due to abnor-
mal rod physiology in the retina and xerophthalmia due to epithelial damage, par-
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