B. N. MAJUMDAR AND S. N. RAY 111
up ; but this assumption is supported by the work of Ranganathan [1941] with rats,
in which he has shown that the withdrawal of calcium from a high fluorine diet led to
early death of the animals and that the toxic effect of fluorine was inversely proportional to the
calcium intake.
Like Ramiah [1941] and Du Toit et al. [1937], we also found that large amounts of
fluorine were being retained from rations containing an appreciable quantity of this
mineral. In the present experiment, the kidneys proved to be the main channel of fluo-
rine excretion which, however, was contrary to-what was observed by Du Toit et al. [1937].
Supplementation of calcium and aluminium salts in the diet increased the amount of
fluorine excreted in faeces, but by only a small amount, the greater portion being still
excreted in urine. This shows that the beneficial effect of calcium phosphate supple-
ment in the first experiment and the protecting action of calcium and phosphorus in pro-
per ratio in three groups of the second set of experiments were not due to the precipi-
tation of fluorine by calcium in the alimentary canal. On the other hand, it will be
noticed that although more fluorine was being retained by the calcium group of animals
in the first experiment, these bulls were better in condition than these in the high fluorine
group. That the evaluation of net retention of fluorine does not give any idea about
the condition of an animal is also seen from the results of the second set of experi-
ments. Here the animals of the calcium group, while losing condition rapidly, were re-
taining about the same quantity of fluorine as the animals in the other groups of this
set. It seems further that bovines behave differently from rats, as in the latter species
the retention of fluorine is depressed by 10 to 12 per cent, when the calcium intake is
increased [Lawrenz and Mitchell, 1941].
The question now arises as to how calcium and phosphorus in adequate quantity and right
proportion help in checking the rapid onset of the toxic effects of fluorine compounds. The
absence of precipitation in the alimentary canal in any significant quantity suggests that the
ingested fluorine must be mobolised somewhere inside the body. It has already been stated
in our previous paper [Majumdar et al, 1943] that extensive periosteal deposits were met with
in the fluorine-fed animals. The formation of these deposits may be nature's attempt to
detoxicate the ingested fluorine by an increased activity of osteoid tissue. This osteogenic
action of fluorine is evident from the better balance of calcium and phosphorus in our low-
fluorine group of animals in the first set, and has also been revealed by the histological
examination of bones of animals suffering from fluorosis [Pande, 1944]. It was also found
by us [Majumdar et al, 1943] that these exostoses contain a very high concentration of fluorine.
The new bone formed under the influence of fluorine feeding is considered to have the com-
position of calcium fluorapatite and is deposited on the outer surface of the pre existing
skeletal tissue. So long as bone-forming minerals, such as calcium and phosphorus, are
supplied in adequate quantities and in proper proportion, the new bone formation and conse-
quent removal (detoxication) of fluorine will proceed smoothly. A metabolism trial in such
circumstances will indicate a high retention of fluorine in a non-toxic form. This was
actually the case in our calcium group of animals (first experiment), as well as in the animals of
the various groups in the second experiment. When, however, fluorine is fed at a very high
level for long periods or when sufficient bone-forming minerals are not present in the feed, or
when these minerals are not in correct proportion, body reserves of calcium and phosphorus
are used up in an attempt to detoxicate the ingested fluorine. This leads to a weakening of
bones, resulting in fractures and other skeletal deformities so often seen in cases of fluorosis.
If fluorine feeding is still persisted in and it no attempt is made to correct the deficiency or
imbalance of calcium and phosphorus, this rate of bone deposition will slow down due to
gradual saturation of bony tissues with fluorine, and consequently much of the ingested
fluorine will escape detoxication, and the concentration of this mineral in the blood will go up.
A portion of this excess fluorine will be excreted through urine, but with the increase in the
blood fluorine concentration, the various soft organs of the body will be acted upon destruc-
tively with the production of syndromes of fluorosis and resulting finally in death. This is
presumably what had happened to the animals of the high fluorine (first experiment) and
calcium (second experiment) groups, as well as in Ranganathan's [1941] rats on a low calcium
diet. It will also be noticed from Tables I and II that the groups showing the most aggravated