686
H O N O R
B . F E L L
A N D
L .
M . R I N A L D I N I
D . E F F E C T S
O N
C E L L F U N C T I O N S , D I F F E R E N T I A T I O N A N D
T H E
B U I L D I N G
O F E X T R A C E L L U L A R M A T E R I A L S
Nutritional requirements in micro-organisms are judged by their
growth curve, but in tissue cells other criteria of response must also be
considered.
It is evident from Reid's (1954) exhaustive review on the influence of
vitamin C on different organs and tissues how little we know about its
action at the cellular level. In an earlier review (1943) she suggested
that ASA might interact with calcium at the cell surface, but the evidence at the time was indirect and inconclusive, and little more has
been done since on the subject.
Nungester and Ames (1948), in well-designed experimental work,
found a correlation between ASA content of leucocytes from peritoneal
exudates and their phagocytic activity and fragility. Regrettably, they
did not investigate the effect of adding ASA and related compounds
to the deficient cells.
The problem of the passage of ASA and D H A across the cell membrane and vascular barriers has been studied by Golden and Sargent
(1952), Raiha (1958), Teruuchi and Mochizuki (1960) and Martin
(1961). The conclusion to be derived from these studies is that D H A
is rapidly converted to ASA after passing the cell membrane. Yet it
seems obvious that ASA and D H A can have different effects on some
cells as evidenced by the fact that D H A can produce diabetes and other
alterations in carbohydrate metabolism which are not produced by
administration of ASA (Meiklejohn, 1953; Stetten and Topper, 1953;
Caramia, 1961).
Chambers and Cameron (1944) studied the effect of corticoids and
vitamin C on the secretory activity of proximal convoluted tubules of
9-day chick mesonephros cultivated in vitro. They found that whole
cortical extract and Kendall's compound E stimulated secretion, but
ASA in concentrations of 100 ^g/ml had no effect. On the other hand,
the same concentration of ASA counteracted the deteriorating effect
of cortical extracts on some embryonic epithelia (Chambers and Cameron, 1943). V o n Mollendorff (1944) found that vitamin C counteracted
the production of mitotic abnormalities elicited in cultures of normal
and malignant tissues by unsaturated steroids. He believed that the
effect was due to reduction of the double bonds.
Freshly isolated myoblasts from heart ventricles and pectoral muscle
of 11-13-day chick embryos could be kept in a good state of functional
differentiation—contraction and beating—for at least 10 days in
Waymouth's medium ' A ' which has no ASA (Rinaldini, 1959) and
in 20% horse serum in which all the ASA has been oxidized beyond
H O N O R
B . F E L L
A N D
L .
M . R I N A L D I N I
D . E F F E C T S
O N
C E L L F U N C T I O N S , D I F F E R E N T I A T I O N A N D
T H E
B U I L D I N G
O F E X T R A C E L L U L A R M A T E R I A L S
Nutritional requirements in micro-organisms are judged by their
growth curve, but in tissue cells other criteria of response must also be
considered.
It is evident from Reid's (1954) exhaustive review on the influence of
vitamin C on different organs and tissues how little we know about its
action at the cellular level. In an earlier review (1943) she suggested
that ASA might interact with calcium at the cell surface, but the evidence at the time was indirect and inconclusive, and little more has
been done since on the subject.
Nungester and Ames (1948), in well-designed experimental work,
found a correlation between ASA content of leucocytes from peritoneal
exudates and their phagocytic activity and fragility. Regrettably, they
did not investigate the effect of adding ASA and related compounds
to the deficient cells.
The problem of the passage of ASA and D H A across the cell membrane and vascular barriers has been studied by Golden and Sargent
(1952), Raiha (1958), Teruuchi and Mochizuki (1960) and Martin
(1961). The conclusion to be derived from these studies is that D H A
is rapidly converted to ASA after passing the cell membrane. Yet it
seems obvious that ASA and D H A can have different effects on some
cells as evidenced by the fact that D H A can produce diabetes and other
alterations in carbohydrate metabolism which are not produced by
administration of ASA (Meiklejohn, 1953; Stetten and Topper, 1953;
Caramia, 1961).
Chambers and Cameron (1944) studied the effect of corticoids and
vitamin C on the secretory activity of proximal convoluted tubules of
9-day chick mesonephros cultivated in vitro. They found that whole
cortical extract and Kendall's compound E stimulated secretion, but
ASA in concentrations of 100 ^g/ml had no effect. On the other hand,
the same concentration of ASA counteracted the deteriorating effect
of cortical extracts on some embryonic epithelia (Chambers and Cameron, 1943). V o n Mollendorff (1944) found that vitamin C counteracted
the production of mitotic abnormalities elicited in cultures of normal
and malignant tissues by unsaturated steroids. He believed that the
effect was due to reduction of the double bonds.
Freshly isolated myoblasts from heart ventricles and pectoral muscle
of 11-13-day chick embryos could be kept in a good state of functional
differentiation—contraction and beating—for at least 10 days in
Waymouth's medium ' A ' which has no ASA (Rinaldini, 1959) and
in 20% horse serum in which all the ASA has been oxidized beyond