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PubMed1981

Influence of chronic ascorbic acid deficiency and excessive ascorbic acid intake on bile acid metabolism and bile composition in the guinea pig.

The influence of chronic ascorbic acid (AA) deficiency and excessive ascorbate consumption on bile acid metabolism, liver and plasma cholesterol levels, hepatic microsomal cytochromes and biliary lipid composition was investigated. Male weanling guinea pigs were fed a cereal-based scorbutigenic diet supplemented with four levels of AA for 7 weeks: deficient, 15 and 30 mg/kg; control, 500 mg/kg; and excess, 20,000 mg/kg. Bile acid kinetic parameters were determined following the intraperitoneal administration of [24-14C] chenodeoxycholic acid. Dietary extremes of AA caused similar alterations in the parameters studied. Relative to the control group, the deficient and excess groups exhibited reduced cytochrome P-450 concentration, lower cholesterol 7 alpha-hydroxylase activity, lower bile acid turnover rate, prolonged bile acid half-life and increased plasma and liver cholesterol concentrations. Deficient and excess groups also exhibited lower biliary cholesterol saturation (i.e., increased bile acid-neutral sterol ratios) than controls. Urinary bile acid excretion was 2- to 3-fold higher in excess guinea pigs than in the other three groups. The data demonstrate the exceptional susceptibility of cholesterol 7 alpha-hydroxylase activity to alteration by dietary extremes of AA, resulting in marked inhibition of bile acid synthesis and elevation of cholesterol levels by both inadequate and excessive AA intake.

Animals↗

PubMed1990

Ascorbic acid deficiency and hepatic UDP-glucuronyl transferase. Qualitative and quantitative differences.

The effect of dietary ascorbate on hepatic UDP glucuronyltransferase (UDPGT) appears to be selective in that only certain isozymes of UDPGT are jeopardized. In this study, ascorbic acid deficiency produced a 68% reduction in the specific activity of hepatic UDPGT towards p-nitrophenol. Earlier studies showed a reduction in UDPGT activity towards p-aminophenol in ascorbate-deficient guinea pigs, whereas bilirubin and acetaminophen glucuronidation were unaffected. Kinetic studies suggest that p-aminophenol and p-nitrophenol are metabolized by a single isozyme in that p-nitrophenol was found to be a competitive inhibitor of p-aminophenol glucuronidation. Both qualitative and quantitative studies on partially purified UDPGT from ascorbate-deficient and ascorbate-supplemented guinea pigs were carried out to investigate the biochemical role of the vitamin. Qualitative differences were observed in UDPGT from ascorbate-deficient animals and included an increased lability to: thermal inactivation; storage at 4 degrees; and purification with UDP-glucuronic acid agarose column chromatography. Furthermore, an analysis of the microsomal membrane showed a 14% increase in membrane fluidity in ascorbate deficiency. Ascorbic acid added in vitro could not reverse the increase in fluidity observed in ascorbate-deficient microsomal membranes; however, ascorbylpalmitate, a more lipophilic form of the vitamin, was effective. Palmitic acid had no effect on membrane fluidity in microsomes from either the ascorbate-supplemented or ascorbate-deficient animals. This increase in membrane fluidity could not be explained by differences in cholesterol, total phospholipid, or phosphatidylcholine content of hepatic microsomes. Furthermore, a quantitative reduction in UDPGT partially purified from ascorbate-deficient guinea pigs was indicated by a marked reduction in protein banding at 55,000 daltons when compared to UDPGT partially purified from ascorbate-supplemented animals.

Animals↗

PubMed1975

Changes relevant to catecholamine metabolism in liver and brain of ascorbic acid deficient guinea-pigs.

A chronic deficiency of ascorbic acid was induced in guinea pig. The level of catecholamines, copper and the activities of ceruplasmin, catecholamine oxidase, monoamineoxidase and acetylcholinesterase were checked in brain, liver and serum. Also the levels of ascorbic acid and glutathione were measured in the organs of ascorbic acid-deficient animals. The most important changes due to the ascorbic acid deficiency were observed in the brain were monoamineoxidase, catecholamineoxidase, acetylcholinesterase and the concentration of catecholamines were altered. The statement that brain is the organ most affected by the ascorbic acid deficiency is discussed.

Acetylcholinesterase↗

PubMed2003

Increase in tartrate-resistant acid phosphatase of bone at the early stage of ascorbic acid deficiency in the ascorbate-requiring Osteogenic Disorder Shionogi (ODS) rat.

The effect of ascorbic acid deficiency on bone metabolism was evaluated using the ascorbate-requiring Osteogenic Disorder Shionogi (ODS) rat model. Ascorbic acid (Asc)-deficient rats gained body weight in a manner similar to Asc-supplemented rats (control) during 3 weeks, but began to lose weight during the 4th week of Asc deficiency. The tartrate-resistant acid phosphatase (TRAP) activity in serum increased to about 2-fold the control value in the rats fed the Asc-free diet for 2, 3, and 4 weeks (AscD2, AscD3, and AscD4), while a decrease in the alkaline phosphatase (ALP) activity was observed only in AscD4 rats. The serum pyridinoline cross-linked carboxyterminal telopeptide of type I collagen (ICTP) level significantly increased to 1.3-, 1.4-, and 1.9-fold of that in the controls in AscD2, D3, and D4, respectively. The ALP activity in the distal femur was unchanged in AscD1, D2, and D3, but decreased to 50% of the control level in AscD4 rats. The TRAP activity in the distal femur increased to about 2-fold of that in the controls in the AscD2 and D3 and decreased to the control level in the AscD4 rats. The amount of hydroxyproline in the distal femur significantly decreased to about 80%, 70%, and 60% of the control in AscD2, D3, and D4 rats, respectively. These decreases were associated with a similar reduction in the calcium content of the distal femur. Histochemical analysis of the distal femur showed an increase in TRAP-positive cells in AscD2 and AscD3 rats and a decrease in the trabecular bone in AscD2, D3, and D4 rats. These results suggested that a deficiency of Asc stimulated bone resorption at an early stage, followed by a decrease in bone formation in mature ODS rats which already had a well-developed collagen matrix and fully differentiated osteoblasts.

Acid Phosphatase↗

PubMed2003

Changes in catecholamine metabolism by ascorbic acid deficiency in spontaneously hypertensive rats unable to synthesize ascorbic acid.

We have previously reported the establishment of a novel rat strain, SHR-od, with both spontaneous hypertension and a defect of ascorbic acid biosynthesis. Blood pressure in mature SHR-od fed an ascorbic acid-supplemented diet is over 190-200 mmHg, while it decreased to around 120 mmHg at 4-5 weeks after the cessation of ascorbic acid supplementation. With regard to possible mechanisms of blood pressure lowering, we focused on catecholamine synthesis in adrenal glands, since catecholamine is a major factor for blood pressure regulation and ascorbic acid is a co-factor of dopamine beta-hydroxylase (DBH) in catecholamine biosynthesis. Male SHR-od (25-week-old) and normotensive ODS rats with a defect in ascorbic acid biosynthesis (25-week-old) were fed a Funabashi-SP diet with or without ascorbic acid (300 mg/kg diet) for 28 days or 35 days. In SHR-od, systolic blood pressure (191 +/- 6 mmHg) began to decrease from day 21 in the ascorbic acid-deficient group, whereas no significant difference was found in ODS rats. In spite of significant lowering of blood pressure, no significant differences were found in catecholamine levels in serum, adrenal glands and brain on day 28. On day 35, however, urinary excretion of norepinephrine and epinephrine in the ascorbic acid-deficient SHR-od were higher at 490% (P < 0.05) and 460% (P < 0.05) of the respective control. Serum catecholamine concentrations and the adrenal catecholamine content tended to be higher in the ascorbic acid-deficient SHR-od than the control of SHR-od and reached to similar level in ODS rats. The administration of ascorbic acid (intraperitoneal injection, 60 mg ascorbic acid/kg body weight, once a day) to the ascorbic acid-deficient SHR-od restored blood pressure to the range 180-190 mmHg within two days. These findings indicate that ascorbic acid deficiency affects catecholamine metabolism in the adrenal glands of SHR-od in response to blood pressure lowering, suggesting catecholamines are not involved in the mechanism for the remarkable reduction in blood pressure in response to ascorbic acid deficiency.

Adrenal Glands↗

PubMedDate not supplied

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

Ascorbic acid is essential to the biosynthesis of collagen, the major organic matrix component of dentine. The ODS rat is a mutant strain of Wistar rat characterized by hereditary lack of L-gulono-gamma-lactone oxidase and thus is unable to synthesize ascorbic acid. ODS rats were given an ascorbic acid-free diet to investigate how ascorbic acid deficiency affects dentine formation in vivo. Histomorphometric analysis on their growing molars and incisors showed a significant reduction in both size and mineral apposition rate of dentine, as revealed by contact microradiography and fluorescent time-marking, respectively. A similar reduction in bone formation was simultaneously demonstrated in the mandible, confirming the previously reported osteopathic effects of ascorbic acid deficiency. When pulp inflammation was induced in lower first molars by making unsealed pulp exposures, specimens from control animals showed continuous deposition of an osteodentine-like tissue in the radicular pulp chamber; this type of mineralized tissue formation was greatly reduced in ascorbic acid-deprived animals. These results indicate that ascorbic acid deficiency hampers dentine formation under both physiological and pathological conditions of the dentine/pulp complex. ODS rats could be useful in investigating in vivo effects of ascorbic acid deficiency on the formation of dentine and other dental mineralized tissues.

Animals↗

PubMed1987

Flavin-containing monooxygenase and ascorbic acid deficiency. Qualitative and quantitative differences.

Ascorbic acid deficiency causes qualitative and quantitative differences in the guinea pig hepatic flavin-containing monooxygenase (FMO). Kinetic studies with purified FMO indicated no significant change in the apparent Km of dimethylaniline or NADPH in ascorbate-supplemented or -deficient animals. Following purification of ascorbate-deficient guinea pig FMO by DEAE-cellulose and blue agarose chromatography, exogenous FAD was required for 15% of the FMO microsomal activity recovered. In contrast, only 5% of the total microsomal enzyme recovered from ascorbate-supplemented animals required exogenous FAD. Furthermore, there was an enhanced sensitivity to time-dependent nonlinearity with the purified ascorbate-deficient guinea pig FMO. The degree of time-dependent nonlinearity was related to the concentration of substrate. Also, purified ascorbate-supplemented guinea pig FMO was stable for 4 weeks at -20 degrees, whereas the ascorbate-deficient enzyme was inactivated. A decrease in the quantity of ascorbate-deficient guinea pig FMO compared to ascorbate-supplemented was indicated by a marked reduction in total FMO activity recovered from blue agarose chromatography and reduced protein staining intensity with SDS-PAGE at 56,000 daltons.

Animals↗

PubMed1977

Phagocytosis and leukocyte enzymes in ascorbic acid deficient guinea pigs.

Enzymes related to bactericidal activities of leukocytes were studied in ascorbic acid deficient guinea pig leukocytes. The activities of glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase were not affected either under resting or phagocytizing conditions in ascorbic acid deficiency. Granule bound NADPH-oxidase activity of resting leukocytes also was not altered in ascorbic acid deficiency. However, the extent of stimulation in NADPH-oxidase activity under phagocytizing condition was found to be significantly lower in ascorbic acid deficient leukocytes than that in control leukocytes. Similary, the extent of release of acid phosphatase from lysosomes during phagocytosis was also low in ascorbic acid deficient leukocytes. Ascorbic acid deficiency did not influence the activities of glutathione reductase and myeloperoxidase of leukocytes. The significance of these enzyme changes is discussed in relation to the decreased phagocytic and bactericidal activities of leukocytes in ascorbic acid deficiency.

Acid Phosphatase↗

PubMed2001

Effect of prolonged marginal ascorbic acid deficiency on lenticular levels of antioxidants and lipid peroxide in guinea pigs.

We examined the effect of prolonged marginal ascorbic acid deficiency of the levels of antioxidants and lipid peroxide in lenses of guinea pigs in order to clarify lenticular antioxidant status under ascorbic acid deficiency. Male guinea pigs aged 4 weeks were given a scorbutic diet (20 g/animal per day) with either marginally deficient ascorbic acid (0.5 mg/animal per day) or sufficient ascorbic acid (1 g/animal per day) in drinking water for 3 and 6 months. The deficient group showed no lens opacity during the administration period. The deficient group had 62.3 and 53.9% of lenticular ascorbic acid content in the sufficient group at 3 and 6 months of ascorbic acid deficiency, respectively. There were no differences in lenticular contents of reduced glutathione and thiobarbituric acid reactive substances, an index of lipid peroxidation, between both groups at 3 and 6 months of ascorbic acid deficiency, while the deficient group tended to have higher lenticular vitamin E content than the sufficient group. The deficient group had higher serum vitamin E concentration than the sufficient group at 3 and 6 months of ascorbic acid deficiency. These results indicate that lenticular antioxidant status is maintained well in guinea pigs with prolonged marginal ascorbic acid deficiency, which may result in no cataract formation.

Animals↗

PubMed2002

Prolonged marginal ascorbic acid deficiency induces oxidative stress in retina of guinea pigs.

We examined whether prolonged marginal ascorbic acid deficiency induces oxidative stress in the retina of guinea pigs. Male guinea pigs aged four weeks were given a scorbutic diet (20 g/animal per day) with either marginally deficient ascorbic acid (0.5 mg/animal per day) or adequate ascorbic acid (1 g/animal per day) in drinking water for three and six months. The retinal contents of the reduced form of ascorbic acid in the deficient group at three and six months were 68.1 and 43.5%, respectively, of that in the corresponding adequate group. The retinal contents of the oxidized form of ascorbic acid in the deficient group at three and six months were 1.9- and 2.7-fold, respectively, higher than that in the corresponding adequate group. The content of retinal thiobarbituric acid reactive substances (TBARS), an index of lipid peroxidation, in the deficient group was 2.5-fold higher than that in the adequate group at six months. The retinal contents of reduced glutathione (GSH) in the deficient group at three and six months were 84.8 and 66.7%, respectively, of that in the corresponding adequate group. The deficient group had 37.5% of retinal vitamin E content of the adequate group at six months. The deficient group had higher serum vitamin E concentration than the adequate group in both experimental periods. There were no differences in serum TBARS and GSH concentrations between the groups at both periods. These results indicate that prolonged marginal ascorbic acid deficiency induces oxidative stress in the retina of guinea pigs without systemic oxidative stress.

Animals↗

PubMed1982

Human T-cell function in experimental ascorbic acid deficiency and spontaneous scurvy.

Studies in animal models suggest that ascorbic deficiency impairs T-cell-mediated immunity. We studied five normal volunteers hospitalized on a metabolic unit and consuming a strictly controlled diet deficient in ascorbic acid I) after a 5-wk control period of ascorbic acid supplementation (75 mg/day) and 2) after a 9-wk period of no supplementation. Three of the subjects were restudied after a 5-wk period of ascorbic acid supplementation after the deficient period. At the end of both control periods ascorbic acid levels in plasma ranged from 0.9 to 1.3 mg/dl and in leukocytes from 19 to 30 microgram/10(8) cells. At the end of the deficient period levels of ascorbic acid in plasma ranged from 0.09 to 0.15 mg/dl and in leukocytes from 6.2 to 10 microgram/10(8) cells, levels at or below those frequently found in frank scurvy. None of the T-cell parameters tested including mitogen responsiveness to phytohemagglutinin and percentage of T-cells bearing receptors for IgM (helper cells) and IgG (suppressor cells) was different in the deficient period compared to the control periods. One patient with spontaneous scurvy (plasma ascorbic acid 0.07 mg/dl, leukocytic ascorbic acid 4.9 microgram/10(8) cells) was studied at the time of admission and after vigorous ascorbic acid repletion. All T-cell parameters after repletion were unchanged from admission. We conclude that in man ascorbic acid deficiency, even at the scorbutic level, does not alter T-cell numbers or impair in vitro T-cell function.

Adult↗

PubMed1982

Lack of effect of subclinical ascorbic acid deficiency upon antipyrine metabolism in man.

The influence of experimentally induced subclinical ascorbic acid deficiency upon antipyrine metabolism was assessed in five healthy male volunteers maintained in a hospital metabolic ward and fed a controlled diet deficient in ascorbic acid. Antipyrine pharmacokinetic parameters were determined four times during the study: at the end of an initial control period, after 28 and 63 days of depletion, and at the end of a second control period. No differences in antipyrine metabolism were observed despite the fact that the subjects had plasma ascorbate levels indicative of vitamin C deficiency (i.e., plasma levels less than 0.3 mg/dl) for 5 days (28 day-depletion) or 40 days (63 day-depletion). This experiment demonstrates that pronounced ascorbic acid deficiency of relatively short duration does not alter antipyrine metabolism in man.

Adult↗

PubMed1994

Ascorbic acid deficiency in guinea pigs: contrasting effects of tissue ascorbic acid depletion and of associated inanition on status indices related to collagen and vitamin D.

To investigate the sensitivity of guinea pig tissues to ascorbic acid depletion, as distinct from inanition, young male guinea pigs were maintained with either ascorbic acid restriction or total diet restriction for 8 weeks. One group (A) received no ascorbic acid for 3 weeks, then 0.5 mg/d for 5 weeks; one group (B) was weight-matched by restricted food intake to the first group; a third (marginally deficient) group (C) received 1 mg ascorbic acid/d throughout; a fourth was weight-matched to this group (D); and a fifth group received the control diet ad lib. (E). Both of the groups with restricted ascorbic acid intakes (A and C) developed very low tissue ascorbic acid contents, but only the first group (severely deficient group A) also exhibited a severely reduced growth rate. This group also exhibited reduced femur calcium and hydroxyproline contents and reduced skin hydroxyproline content. These changes were not seen in the corresponding weight-matched group (B). Neither plasma alkaline phosphatase (EC 3.1.3.1) activity, nor a variety of indices of vitamin D status exhibited changes which could be attributed specifically to reduced ascorbic acid intake and hence to lowered tissue ascorbic acid content. It is concluded that low tissue ascorbic acid levels in guinea pigs clearly alter the connective tissue composition of growing femur and skin, but do not necessarily produce a major, specific effect on vitamin D status. Moreover, the control of inanition is crucial to permit interpretation of the changes in metabolism that are caused by ascorbic acid deficiency.

Alkaline Phosphatase↗

PubMed1997

Ascorbic acid deficiency decreases the renal level of kidney fatty acid-binding protein by lowering the alpha2u-globulin gene expression in liver in scurvy-prone ODS rats.

The evidence for the role of ascorbic acid in gene expression or protein synthesis in vivo is limited. To investigate this role of ascorbic acid, we surveyed proteins whose tissue levels are changed by ascorbic acid deficiency by using ODS rats with a hereditary defect in ascorbic acid biosynthesis. Male ODS rats (7 wk old, body weight approximately 130 g) were fed a basal diet containing ascorbic acid (300 mg/kg diet) or an ascorbic acid-free diet for 14 d. Ascorbic acid deficiency decreased a renal protein with an apparent molecular mass of 17 kDa. The amino-terminal amino acid sequence of 16 residues of this 17-kDa protein was identical to a kidney fatty acid-binding protein known to be generated by proteolytic degradation of alpha2u-globulin, a major urinary protein of adult male rats. alpha2u-Globulin is synthesized in liver, secreted into blood and excreted into urine, but partially reabsorbed by renal proximal tubules. It exists in kidney in a proteolytically modified form. Ascorbic acid deficiency lowered the renal level of kidney fatty acid-binding protein to 53% (P < 0.05) and lowered the serum level of alpha2u-globulin to 52% (P < 0.05) of the level of the control group, but did not affect the amount of alpha2u-globulin excreted into urine. The hepatic level of alpha2u-globulin mRNA of the ascorbic acid-deficient rats was significantly lower (30%) than that of the control rats. These results suggest that in male ODS rats, ascorbic acid deficiency decreases the renal level of kidney fatty acid-binding protein by lowering alpha2u-globulin gene expression in liver.

Alpha-Globulins↗

PubMed1991

Ascorbic acid deficiency elevates serum level of LDL-cholesterol in a rat mutant unable to synthesize ascorbic acid.

The effect of ascorbic acid deficiency on serum levels of high density lipoprotein- (HDL-), low density lipoprotein- (LDL-), very low density lipoprotein- (VLDL-) and chylomicron-cholesterol was examined in ODS-od/od rat (ODS rat), that is a rat mutant unable to synthesize ascorbic acid. Male ODS rats were fed an ascrobic acid-free diet for 20 days. In another two groups, the diet supplemented with 300 mg ascorbic acid/kg diet was fed either ad libitum (ad libitum control) or in pair-feeding (pair-fed control). Pair-fed rats received the same amount of diet as rats fed the ascorbic acid-free diet. Serum level of total cholesterol in the ad libitum control rats, ascorbic acid-deficient rats, and the pair-fed control rats were 100.1 +/- 8.4 mg/dl, 92.8 +/- 6.2 mg/dl and 72.2 +/- 4.8 mg/dl, respectively. The level of LDL-cholesterol in ascorbic acid-deficient rats was significantly higher than that in the ad libitum control or that in the pair-fed control. The level of HDL-cholesterol in ascorbic acid-deficient rats was lower than that in the ad libitum control, but was not changed as compared with that in the pair-fed control. Ascorbic acid deficiency did not affect serum level of VLDL-cholesterol or chylomicron-cholesterol as compared with those in the controls. These results demonstrate that ascorbic acid deficiency causes the elevation of serum level of LDL-cholesterol both in ad libitum feeding condition and pair feeding condition.

Animals↗

PubMed1992

Examination for lipid peroxidation in liver microsomes of guinea pigs as a causal factor in the decrease in the content of cytochrome P-450 due to ascorbic acid deficiency.

The content of cytochrome P-450 in liver microsomes from guinea pigs was decreased by ascorbic acid-deficiency. Since ascorbic acid is an antioxidant in vivo, the possible involvement of lipid peroxidation in this phenomenon was investigated. In fact, the level of lipid peroxides in liver homogenates of guinea pigs was increased by ascorbic acid deficiency. The level was significantly decreased when the animals were given tocopherol acetate (25 mg/kg/day, s.c.) with an ascorbic acid-free diet. The activities of aminopyrine N-demethylase, aniline hydroxylase, p-nitroanisole O-demethylase and 7-ethoxycoumarin O-deethylase, and the content of cytochrome P-450 spectrally determined did not restore the control level by the administration of tocopherol acetate to the ascorbic acid-deficient animals. Western blot analysis of liver microsomes with antibodies to rat P-450IA2 (P-448-H), P-450IIB1 (P-450b) and human P-450IIIA4 (P-450NF) showed that ascorbic acid-deficiency resulted in a decrease in the amount of cytochrome P-450 immunochemically related to P-450IA2, but not the amounts of the forms of cytochrome P-450 cross-reactive with antibodies to P-450IIB1 and P-450IIIA4. The reduced amounts of cytochrome P-450 cross-reactive with antibodies to rat P-450IA2 in liver microsomes of ascorbic acid-deficient animals remained unchanged even when lipid peroxidation was inhibited by tocopherol acetate, suggesting that there is a mechanism(s) other than lipid peroxidation involved in the reduction of amounts of cytochrome P-450 by ascorbic acid deficiency.

7-Alkoxycoumarin O-Dealkylase↗

PubMed1983

Effects of ascorbic acid deficiency on the in vitro biosynthesis of cyclooxygenase metabolites in guinea pig lungs.

Endogenous levels of ascorbic acid may play a role in regulating the biosynthesis of cyclooxygenase metabolites in lungs of male guinea pigs. The in vitro biosyntheses of prostaglandins, prostacyclin and thromboxane were examined using isolated microsomal membranes from control and ascorbic acid deficient guinea pigs, under conditions in which the substrate concentration ( [3H]-arachidonic acid) was varied from 10-100 microM. Maintenance of guinea pigs for two weeks on an ascorbic acid deficient diet did not alter lung/body weight ratios, nor protein content of the lungs. Lung microsomes from ascorbic acid deficient guinea pigs demonstrated a greater biosynthesis of total cyclooxygenase metabolites at low substrate concentrations. A significant increase in the PGF2 alpha synthesis was observed in the scorbutic microsomes at 20 microM arachidonic acid. At higher substrate concentrations the production of PGF2 alpha was significantly reduced in ascorbic acid deficient animals. By contrast, biosynthesis of thromboxane or prostacyclin in treated animals was not significantly different from control microsomes. At a substrate concentration of 100 microM, there was equivalent synthesis of total cyclooxygenase metabolites in control and vitamin C deficient animals. The changes in prostaglandin biosynthesis were not due to an interaction of ascorbic acid with glutathione levels in the lung. These results support the hypothesis that ascorbic acid may modulate cyclooxygenase activity in the lung in a substrate dependent nature.

Animals↗

PubMed2004

Short-term ascorbic acid deficiency does not impair antioxidant status in lens of guinea pigs.

We examined whether short-term ascorbic acid deficiency impairs antioxidant status in the lens of guinea pigs. Male guinea pigs aged 4 wk were given a scorbutic diet (20 g/animal per day) with and without ascorbic acid (400 mg/animal per day) in drinking water for 3 wk. The ascorbic acid-deficient group showed no lens opacity. The ascorbic acid-deficient group had 14% of serum ascorbic acid concentration, 6% of aqueous humor ascorbic acid concentration, and 18% of lens ascorbic acid content in the ascorbic acid-adequate group. There were no differences in the contents of lens reduced glutathione and thiobarbituric acid reactive substances, an index of lipid peroxidation, between the ascorbic acid-deficient and adequate groups, while the deficient group had higher lens vitamin E content than the adequate group. The ascorbic acid-deficient group had higher serum vitamin E concentration than the ascorbic acid adequate group, while there were no differences in the concentrations of serum reduced glutathione and tiobarbituric acid reactive substances between the deficient and adequate groups. These results indicate that short-term ascorbic acid deficiency does not impair antioxidant status in the lens of guinea pigs despite induction of severe ascorbic acid depletion in the tissue, which may result in no cataract formation.

Animals↗