Dietary Concentrations Of Vitamin Research Articles

Nutrition and Equine Performance

Some aspects of energy, protein and vitamin E nutrition of the performance horse are discussed. The amount, dietary source and time of ingestion of energy before exercise can influence performance. In 1989 the National Research Council (NRC) increased their estimates of energy required by racehorses. Recent studies indicate that the increase was reasonable. Many factors, however, can influence energy requirements. Therefore, the best measure would be body weight and composition of the horse. A proper balance of soluble carbohydrate, fiber, fat and protein is essential. Some guidelines are presented. The amount and type energy source given before exercise can influence level of plasma glucose and free fatty acids during exercise, but the effects of these changes in the concentration of metabolites remains to be determined. There is no evidence that increased dietary concentrations of protein are needed and, in fact, may impair performance. Supplemental histidine (to enhance carnosine levels) or carnitine appear to be of limited value for horses fed conventional diets. Dietary concentrations of vitamin E less than the 80 IU/kg recommended by NRC seem to adequately protect against exercise-induced peroxidation. The NRC value may be justified on the basis of immune response, but further studies are needed. Vitamin E has been shown to be involved with familial equine degenerative myeloencephalopathy and may be involved with equine motor neuron disease, a condition considered to be similar to amyotrophic lateral sclerosis in humans.

Dietary vitamin D supplementation attenuates immune responses of pigs challenged with rotavirus potentially through the retinoic acid-inducible gene I signalling pathway.

In the present study, twenty-four Duroc × Landrance × Yorkshire (initial body weight (BW) of 21·82 (sem 2·06) kg) cross-bred pigs were used to determine whether dietary vitamin D supplementation could confer protection against viral infections through the retinoic acid-inducible gene I (RIG-I) signalling pathway in pigs. Experimental treatments were arranged in a 2 × 2 factorial manner with the main effects of immune challenge (control v. porcine rotavirus (PRV) challenge) and dietary concentrations of vitamin D (200 and 5000 IU; where 1 IU of vitamin D is defined as the biological activity of 0.025 mg of cholecalciferol). The pigs were fed a diet containing 200 or 5000 IU vitamin D in the first week of the study period. On day 8, the pigs were orally dosed with 4 ml of Dulbecco's modified Eagle's medium/Ham's F-12 medium containing PRV or essential medium (control). Serum samples were collected on day 8 (pre-challenge), and 6 d after the PRV challenge, the pigs were killed to evaluate intestinal morphology and tissue gene expression following the last blood collection. Pigs challenged with PRV had decreased BW gain (P< 0·01), feed intake (P< 0·01), villus height (P< 0·01), faecal consistency (P< 0·05), and serum 1,25-dihydroxyvitamin D concentration (P< 0·01) and increased (P< 0·01) serum IL-2, IL-6 and interferon (IFN)-β concentrations. Vitamin D supplementation mitigated these effects. The mRNA expression of RIG-I (P< 0·01), IFN-β promoter stimulator 1 (P< 0·01), IFN-β (P< 0·01) and interferon-stimulated gene 15 (ISG 15 ) (P< 0·01) was up-regulated by the PRV challenge and vitamin D supplementation in the intestine. In conclusion, vitamin D supplementation could activate the RIG-I signalling pathway and thus alleviate the negative effects caused by PRV challenge.

Restriction of vitamin A and D in beef cattle finishing diets on feedlot performance and adipose accretion1

Feedlot producers often exceed NRC recommendations for vitamin A and D supplementation; however, increased concentrations of these vitamins have been shown to limit adipocyte differentiation in vitro. A feedlot trial was conducted using 168 Angus crossbred steers (BW = 284 ± 0.4 kg) allotted to 24 pens. The experiment had a 2 × 2 factorial arrangement of treatments: no supplemental vitamin A or D (NAND), 3,750 IU vitamin A/kg dietary DM with no supplemental vitamin D (SAND), no supplemental vitamin A and 1,860 IU vitamin D/kg dietary DM (NASD), and 3,750 IU and 1,860 IU vitamin A and D/ kg dietary DM (SASD), respectively. Serum, liver, and intramuscular and subcutaneous adipose tissue retinol concentrations were decreased in (P < 0.001) in cattle fed the no supplemental vitamin A diets (NAND and NASD combined) compared with those consuming supplemental vitamin A (SAND and SASD combined) diets. In addition, intramuscular retinol concentration was 38% less than in the subcutaneous depot. Serum 25(OH)D(3) concentrations were reduced (P < 0.001) during the first 70 d when cattle were fed no supplemental vitamin D diets (NAND and SAND combined); however, liver 25(OH)D(3) concentrations remained unchanged (P > 0.10) through d 184. Serum and liver 25(OH)D(3) concentrations increased (P < 0.001) with vitamin D supplementation (NASD and SASD combined). The DMI, ADG, G:F, and morbidity were not affected (P > 0.10) by dietary concentration of vitamin A or D. There were vitamin A and D interactions (P < 0.03) for backfat thickness and USDA Yield grade. Cattle fed the NAND diet had greater (P < 0.03) Yield grades than other treatments because of greater (P < 0.005) 12th rib backfat thickness in NAND steers than the NASD and SAND steers. Vitamin D concentrations were attenuated and minimal carcass adiposity responses to vitamin D supplementation were observed. Feeding a diet without supplemental vitamin A increased (P < 0.05) Quality grades and marbling scores and tended (P = 0.06) to increase ether extractable lipid of the LM. As retinol and 25(OH)D(3) concentrations in feedlot cattle declined as a result of a lack of dietary supplementation, adipose accretion increased, resulting in elevated Quality and Yield grades. Withdrawal of supplemental vitamin A, D, or both from the finishing diet of feedlot beef cattle had minimal impact carcass composition.

Growth Performance, Immune Response, and Resistance toStreptococcus iniaeof Nile Tilapia,Oreochromis niloticus, Fed Diets Containing Various Levels of Vitamins C and E

Growth, immunity, and resistance of Nile tilapia to Streptococcus iniae challenge were evaluated after feeding diets supplemented with vitamin C (0, 100, 2000 mg/kg) and E (0, 50, 500 mg/kg) for 12 wk. Supplementation of 100 mg vitamin C/kg to the basal diet was sufficient to increase growth and feed efficiency. The amount of vitamin E present in the basal diet (23.1 mg/kg) was sufficient to promote good growth and feed efficiency, but adding 50 mg vitamin E/kg was necessary to increase survival. Liver vitamin C and E concentrations increased with increasing dietary concentrations of the corresponding vitamin. Dietary vitamin E concentrations had no effect on liver vitamin C concentration, but increasing dietary vitamin C increased liver vitamin E. Although hematology was generally unaffected by dietary vitamin E, significantly lower red blood cell count and hemoglobin and higher mean corpuscular volume were observed in fish fed the vitamin C-unsupplemented diets. Total immunoglobulin and lysozyme activity were significantly higher and lower, respectively, in fish fed 2000 mg/kg vitamin C diets. Vitamin E at 500 mg/kg diet significantly decreased alternative complement activity. Dietary concentrations of vitamin C had no effect on mortality following S. iniae challenge, but mortality significantly decreased in fish fed vitamin E–supplemented diets.

Effects of concentrations of cyanocobalamin in the gestation diet on some criteria of vitamin B12 metabolism in first-parity sows1,2

In swine nutrition, little is known about the role of vitamin B(12) in the reproductive processes. The current study was undertaken to obtain information on the dose-response pattern of different metabolic criteria related to the homeostasis of vitamin B(12) and homocysteine in gestating sows receiving various concentrations of dietary vitamin B(12) (cyanocobalamin). Homocysteine is a detrimental intermediate metabolite of the vitamin B(12)-dependent remethylation pathway of Met. Forty nulliparous (Large White x Landrace) sows were randomly assigned during gestation to dietary treatments containing 5 concentrations of cyanocobalamin (0, 20, 100, 200, or 400 microg/kg). During lactation, a diet containing 25 microg of cyanocobalamin/kg (as-fed) was given to all sows. During gestation, plasma vitamin B(12) increased as concentrations of dietary cyanocobalamin increased (linear and quadratic, P < 0.01) and the effect persisted during lactation (21 d postpartum) both in plasma (linear and quadratic, P < 0.05) and the liver (linear and quadratic, P < 0.04). Plasma homocysteine decreased with concentrations of cyanocobalamin provided to sows during gestation (linear, quadratic, and cubic, P < 0.01). At parturition, vitamin B(12) in colostrum increased as concentrations of cyanocobalamin increased (linear and quadratic, P < 0.01), but the treatment effect persisted (linear, P = 0.01) only up to 1 d postfarrowing. However, in piglets there was no treatment effect (P = 0.59) on plasma vitamin B(12) before colostrum intake, but a linear effect of concentrations of cyanocobalamin (P = 0.04) was observed 1 d later. Plasma homocysteine in piglets during lactation decreased with increasing concentrations of cyanocobalamin given to sows in gestation (linear and quadratic, P < 0.01). Based on a broken-line regression model, the concentrations of dietary cyanocobalamin that maximized plasma vitamin B(12) and minimized plasma homocysteine of sows during gestation were estimated to be 164 and 93 microg/kg, respectively. The maximal residual responses in sows and piglets during lactation were observed with treatments of 100 or 200 microg of cyanocobalamin/kg. The dietary cyanocobalamin concentration necessary to optimize the response of these metabolic criteria remains to be refined within lower and narrower ranges of cyanocobalamin concentrations (i.e., <200 mg/kg). Moreover, the biological significance of such concentrations of cyanocobalamin needs to be validated with performance criteria by using greater numbers of animals during several parities.

Alpha-tocopherol concentrations and case life of lamb muscle as influenced by concentrate or pasture finishing

Two experiments were conducted to evaluate alpha-tocopherol accumulation in muscle of lambs finished on pasture or concentrates. The objective for Exp. 1 was to compare accumulation of alpha-tocopherol in the longissimus muscle of pasture-fed lambs to that of lambs fed three concentrations (15, 150, and 300 IU/kg of DM) of supplemental vitamin E (all rac alpha-tocopheryl acetate) in all-concentrate diets. The objective in Exp. 2 was to investigate the effect of duration of supplemental vitamin E feeding on alpha-tocopherol content and color change during display case storage of lamb muscle. Treatments evaluated in Exp. 2 were: 15 IU of supplemental vitamin E/kg DM fed to finish; 15 IU/kg followed by 300 IU/kg of DM during the last 21 d; and 15 IU/kg DM until 7 d prior to finish, then 300 IU/kg DM. In Exp. 1, alpha-tocopherol concentration of rotational grazed alfalfa and perennial ryegrass averaged 137 and 169 mg/kg of DM. Vitamin E treatments for lambs fed concentrate diets did not affect ADG (P > 0.15), but ADG was greater (P < 0.01) for concentrate-fed lambs than for grazing lambs. For the concentrate-fed lambs, alpha-tocopherol in longissimus muscle increased quadratically (P < 0.05) as dietary concentrations of vitamin E increased. Predicted maximum alpha-tocopherol concentration in muscle occurred at about 400 IU/kg of diet DM. Longissimus muscle from lambs grazing alfalfa or ryegrass had similar (P > 0.50) alpha-tocopherol concentrations, and those concentrations were similar to values obtained when the concentrate diet supplemented with 150 IU of vitamin E/kg was fed. In Exp. 2, no differences (P > 0.10) in ADG were observed. Concentrations of longissimus alpha-tocopherol were highest when 300 IU supplemental vitamin E was fed for 21 d prior to slaughter. During a 6-d display period, semimembranosus steaks from lambs fed 300 IU of supplemental vitamin E/kg for either 7 or 21 d had higher a* and b* color readings than steaks from lambs fed 15 IU/kg of supplemental vitamin E. Increased consumption of vitamin E either via pasture or supplementation results in higher alpha-tocopherol concentrations in meat.

Optimal dietary concentration of vitamin E for alleviating the effect of heat stress on egg production in laying hens

1. The effects of different dietary concentrations of vitamin E (alpha-tocopherol acetate) were investigated on laying hens exposed to chronic heat stress at 32 C from 26 to 30 weeks of age. 2. Diets containing 5 dietary concentrations of vitamin E (a control diet containing 10 mg alpha-tocopherol/kg or this diet supplemented to contain 125, 250, 375 and 500 mg alpha-tocopherol/kg) were fed to 335 birds. Half of the birds received the supplemented diets for only 4 weeks before the heat stress period (short supplementation duration, SSD) and were fed on the control diet for a further 12 weeks. The remaining birds were fed on the supplemented diets throughout the experiment, 4 weeks before, 4 weeks during and 8 weeks after the heat stress period (long supplementation duration, LSD). 3. Egg production was significantly higher during (80.6 vs 68.9%, P <0.02) and after (75.3 vs 62.7%, P <0.02) the period of stress in the LSD group fed on the diet containing 250 mg vitamin E/kg compared with the group fed on the control diet. LSD birds given 375 and 500 mg vitamin E/kg also had higher egg production than control birds during heat stress but the differences failed to reach significance (74.6 vs 68.9% and 77.1 vs 68.9% respectively). In the SSD groups, mean egg production of the birds given the diets supplemented with 125 mg vitamin E/kg or more was significantly different from the control group after heat stress (70.3 vs 62.7%, P <0.05). Egg weight and food intake were similar in all the groups. 4. Plasma and liver vitamin E concentrations were proportional to the vitamin E intake before the stress period, dropped during heat stress in the SSD groups but were maintained at concentrations closer to those observed before heat stress in the LSD groups. 5. It is concluded that a dietary supplement of 250 mg vitamin E/kg provided before, during and after heat stress is optimum for alleviating, at least in part, the adverse effects of chronic heat stress in laying hens.

Modification of postmilking standing time by altering feed availability.

Control of environmental mastitis remains a problem on many modern dairy farms. These infections are often transmitted between milkings, and milking hygiene will not prevent new infection. Consequently, the control of environmental mastitis has prompted dairy managers to develop new approaches that either limit bacterial contamination of teat ends between milkings or directly increase the cow's resistance to infection. Intervention strategies that may decrease the incidence of environmental mastitis include improved sanitation of housing areas, decreased water use in udder preparation, optimal dietary concentrations of vitamin E and selenium, and use of R-mutant vaccines (Smith et al. 1984, 1985; Weiss et al. 1990; Smith &amp; Hogan, 1993; Tyler et al. 1993).Dairy managers are encouraged to provide cows with clean, fresh, palatable feed immediately after milking. This practice is thought to provide cows with an incentive to remain standing for an extended interval, permit teat sphincters to close, and limit teat end contamination and new infections when cows lie down. In one recent study, cows that had access to feed remained standing for a significantly longer time than did cows that were denied access to feed (48 v. 21 min; Tyler et al. 1997). The purpose of the present study was to substantiate that feed availability could be used to extend postmilking standing time in a larger population of cows maintained under different management conditions.

Influence of high dietary vitamin E supplementation on egg production and plasma characteristics in hens subjected to heat stress

1. The effects of different dietary concentrations of vitamin E (alpha-tocopherol acetate) were investigated in 2 experiments on laying hens exposed to chronic heat stress at 32C. 2. In the first experiment, egg production and plasma concentrations of calcium and egg yolk precursors were measured in 24 hens before, during and after a stress period of one week and fed on diets containing 10 or 500 mg vitamin E/kg. 3. In the second, larger experiment, egg production and food intake were measured in 300 hens housed in 2 temperature-controlled rooms and fed on diets containing 10, 125 or 500 mg vitamin E/kg. Birds in room 1 were stressed from 24 to 28 weeks of age and those in room 2 from 32 to 36 weeks. 4. In experiment 1, egg production and egg weight were significantly higher (72.6 vs 51.2%, P < 0.05 and 66.6 vs 63.1 g, P < 0.005 respectively) during and after the period of stress in the group given 500 mg vitamin E/kg. Plasma concentrations of calcium, vitellogenin (zinc) and VLDL (triglyceride) were also higher in this group. 5. In experiment 2, egg production was significantly higher (65.4 vs 56.2%, P < 0.05) during and after the period of heat stress in birds in room 1 fed on the diet containing 500 mg vitamin E/kg. Egg production was also higher (49.9% vs 44.7%) on this treatment during the stress period in room 2, though the difference was not significant (P < 0.10). Egg weight and food intake were unaffected by treatment in either room. 6. It is concluded that dietary supplementation with extra vitamin E can, at least in part, alleviate the adverse effects of chronic heat stress in laying hens, perhaps by maintaining the supply of egg precursors in plasma.

Adverse effects of Escherichia coli infection of turkeys were not alleviated by supplemental dietary vitamin E

Two experiments were conducted to determine the influence of dietary vitamin E on the response of young male turkeys to Escherichia coli infection. A complete factorial arrangement of two concentrations of supplemental dietary vitamin E (12 or 300 IU/kg as dl-alpha-tocopheryl acetate) and infection or no infection of turkeys with E. coli was used in both experiments. In Experiment 1, each dietary treatment was fed to four pens of turkeys from 1 to 28 d of age. At 28 d, turkeys in two pens per dietary treatment received an injection of 3.0 x 10(7) E. coli cells into the left and right thoracic air sacs. All turkeys were necropsied 7 d after E. coli injection and the incidence and severity of lesions in air sacs, lungs, pericardium, and liver were determined. The same dietary vitamin E treatments were used in Experiment 2. Each diet was fed to eight pens of turkeys from 1 to 47 d of age. At 47 d, turkeys in four pens per dietary treatment received an injection of 3.0 x 10(7) cells of the same E. coli used in Experiment 1 into the left and right thoracic air sacs. All turkeys were necropsied as in Experiment 1 at 54 d of age. Weight gain and efficiency of feed utilization were impaired markedly by E. coli infection during the 7 d after injection. Livability also was decreased by E. coli infection in Experiment 1 but not in Experiment 2. Adverse effects of E. coli on performance and livability were not affected by dietary vitamin E concentration. Lesions observed in turkeys that received E. coli injection ranged from mild to severe, with the most severe lesions observed in air sacs. Lung lesions were observed frequently but were less severe than in air sacs. Dietary concentration of vitamin E had no effect on incidence or severity of lesions in air sacs or lungs. Overall, the results of these experiments show that adding 300 IU of vitamin E/kg of diet did not alleviate the adverse effects of E. coli infection in young turkeys.

Influence of vitamin C on the folate requirement of channel catfish, Ictalurus punctatus, for growth, hematopoiesis, and resistance to Edwardsiella ictaluri infection

Channel catfish were fed a semipurified basal diet containing 0, 0.4, or 4.0 mg folic acid/kg with 0, 20, or 200 mg vitamin C/kg in a factorial design in aquaria (29±2°C) for 25 weeks, and growth, survival, and hematological measurements were determined. The remaining fish were overwintered (25 weeks) in circular raceways at ambient outdoor temperature, fed the same experimental diets and challenged with Edwardsiella ictaluri when the water had reached 26°C. Dietary supplementation of folic acid had no effect on any measurement except hematocrit without dietary vitamin C. When the marginal level of vitamin C (20 mg/kg) was fed, hematological measurements increased maximally with the low or high supplement of folic acid (0.4 or 4.0 mg/kg), but weight gain and RBC mean corpuscular volume (MCV) did not respond to folic acid supplementation. When the high level of vitamin C (200 mg/kg) was fed, weight gain improved and MCV decreased maximally with the highest supplement of folic acid. Fish challenged with E. ictaluri showed maximum survival and antibody production when 0.4 or 4.0 mg folic acid/kg was fed with the high level of vitamin C, but only the highest supplement of folic acid improved survival when the diet contained the marginal level of vitamin C. Simultaneous supplementation of both vitamins at the highest levels resulted in the lowest incidence of morphologically abnormal blood cells. These results indicate that the dietary concentration of vitamin C influences the response of channel catfish to different dietary levels of folic acid.

Effect of Vitamin A on longevity

Increasing the dietary content of Vitamin A from inadequate to adequate during the developmental stages of Drosophila increased the median life span by as much as 17.5%. The optimum dietary range of concentrations of Vitamin A for increasing the life span of Drosophila was found to be between 4 and 8 IU/g food. The maximum life span was reduced as dietary concentrations of Vitamin A exceeded this value. Vitamin A palmitate and retinal inhibited the peroxidation of linolenic acid induced by the generation of superoxide radicals from acetaldehyde. Other forms of Vitamin A, such as retinol and retinoic acid, moderately inhibited lipid peroxidation at low concentrations but stimulated peroxidation considerably when present at high concentrations. Based upon the ability of these retinoids to inhibit the reduction of cytochrome c by superoxide radicals, we propose that retinoids can inhibit and stimulate lipid peroxidation depending upon their concentration by reacting with superoxide radicals. We suggest that this reaction is the basis for the apparent ability of Vitamin A to prolong and shorten life span depending upon the dietary intake.

Effect of high concentrations of dietary vitamin E during various age periods on performance, plasma vitamin E and meat stability of broiler chicks at 7 weeks of age.

1. The effect of high concentrations of vitamin E (alpha-tocopheryl acetate) fed during various age periods on the performance and the oxidative stability (thiobarbituric acid [TBA] values) of the drumstick meat of 7-week-old broiler chicks was determined. The basal diets (for the age periods 0 to 3, 3 to 6 and 6 to 7 weeks) contained 60 g soyabean oil and 24 mg vitamin E/kg. The following five treatments were evaluated: (1) the basal diets from 0 to 7 weeks of age (control); (2) vitamin E, 100 mg/kg diet from 0 to 7 weeks of age; (3) vitamin E, 150 mg/kg diet from 0 to 3 weeks of age; (4) vitamin E, 150 mg/kg diet from 0 to 3 weeks of age and 100 mg/kg diet from 6 to 7 weeks of age; (5) vitamin E, 100 mg/kg diet from 5 to 7 weeks of age. 2. Food intake, weight gain and food efficiency were not significantly (P greater than 0.05) affected by the vitamin E treatments. 3. Plasma alpha-tocopherol (AT) concentrations in treatments 2, 4 and 5 were similar, and markedly higher than those in treatments 1 and 3, while those of treatment 3 were significantly (P less than 0.001) higher than those of treatment 1. Plasma retinol concentrations were not significantly (P greater than 0.05) affected by the vitamin E treatments. 4. TBA values of the meat were very low and not significantly affected by the vitamin E treatments. However, after incubation the TBA values were highly significantly (P less than 0.01) negatively correlated with the amount of vitamin E consumed during the experiment. The stability of meat of birds fed the various combinations of vitamin E (treatments 3, 4 and 5) was significantly (P less than 0.05) higher than that of birds which did not receive additional vitamin E (treatment 1), but it was significantly (P less than 0.001) lower than that of birds which received vitamin E continuously (treatment 2). 5. It is concluded that a high concentration of vitamin E fed during 0 to 3 weeks of age may significantly improve AT status of the broiler chick up to 7 weeks of age.

Effect of vitamin E and selenium supplement on the aging peripheral neurons of the male sprague—dawley rat

The effect of life-long diets containing different concentrations of selenium and vitamin E on the age pigment accumulation in the rat superior cervical ganglion, vagal ganglion and dorsal root ganglion, was studied using microspectrofluorometry. All types of ganglia showed unchanged amounts of age pigments at low or hihg concentrations of selenium, whereas dietary concentration of vitamin E regulated age pigment content in the dorsal root ganglion, but not in the superior cervical and vagal ganglion. Vitamin E deficiency induced a three-fold increase in age pigment content in dorsal root ganglion at 8 months of age, whereas high vitamin E concentration was associated with a lesser amount of pigments at 18 months of age. Emission spectra of age pigment recorded from the dorsal root ganglion and vagal ganglion were different from that from the superior cervical ganglion, but were independent of dietary concentrations of selenium or vitamin E. The results suggest that exogenous antioxidants may play a more crucial role in lipid peroxidation and accumulation of age pigment in dorsal root ganglion than in autonomic ganglia.

Effect of Dietary Vitamin E on Platelet Tocopherol Values and 12-Lipoxygenase Activity

This study was designed to evaluate the effects of different amounts of dietary vitamin E on platelet tocopherol levels and 12-lipoxygenase activity when exogenous arachidonic acid was used as substrate. Weanling male Sprague-Dawley rats were fed diets containing 0, 50, and 5000 ppm of D-alpha-tocopherol acetate for 4 months. Platelet tocopherol was increased with increasing concentrations of dietary vitamin E; however, the conversion of exogenously added arachidonate by platelet to 12-HETE (12-hydroxyeicosatetraenoic acid) and thromboxane B2 from these three dietary groups was essentially the same. This study provides direct evidence that platelet 12-lipoxygenase activity is independent of its vitamin E content when exogenously added arachidonate was used as substrate.

The influence of dietary history on the production of free radicals in rat liver microsomes.

Free radicals have been trapped in microsomal fractions from rat livers by the use of alpha-(4-pyridyl-l-oxide)-N-tert-butylnitrone (4-POBN) and detected by ESR spectroscopy. Using this technique we have investigated the effects of low dietary concentrations of vitamin E and selenium (Se) on free radical production. When the microsomal fractions were incubated with Fe, ADP and NADPH significantly greater amounts of radicals were initially trapped when rats were deficient in vitamin E (whether combined with Se deficiency or not) than from Se-deficient animals or Se- and vitamin E-supplemented controls. After prolonged incubation (ca. 30-45 mins) the free radicals trapped from the microsomes from the Se-deficient animals rose to amounts comparable to those seen in the vitamin E-deficient microsomes. Over the same period of incubation approximately half this quantity of radicals were trapped in liver microsomes from Se- and vitamin E-supplemented rats. The effects of 4-POBN on the levels of peroxidation in the various microsomal fractions were assessed by measuring the thiobarbituric acid reactive substances (TBARS). The presence of 4-POBN significantly reduced the amounts of TBARS formed on incubation and there was a clear distinction between the groups on the basis of the vitamin E status of their diets.

Vitamin A status, polybrominated biphenyl (PBB) Toxicosis, and common bile duct hyperplasia in rats

The interaction between dietary concentrations of vitamin A and PBB was evaluated in two experiments. In the first experiment, male weanling rats were used in a 2 × 3 factorial experiment. Concentrations of PBB were 0, 10, or 100 mg/kg of diet and diets were either vitamin A-deficient or were supplemented with 3000 IU vitamin A palmitate/kg of diet. In the second experiment the design was similar except that two vitamin A-supplemented diets were used, one containing 3,000 IU/vitamin A palmitate/kg of diet and the other 30,000 IU. Diets contained either 0 or 100 mg of PBB/kg. Clinical signs of vitamin A deficiency and mortality occurred early in rats fed vitamin A-deficient diets containing 100 mg of PBB/kg. Vitamin A supplementation provided partial protection against decreased weight gain associated with PBB. Decreases in thymic weight associated with PBB toxicosis were prevented by supplementation with vitamin A. Massive enlargement of the common bile duct occurred in rats fed a vitamin A-deficient diet containing 100 mg of PBB/kg. Histologically, this lesion consisted of extensive hyperplasia. A significant decrease in retinol concentrations in the sera was recorded in rats fed vitamin A-deficient diets containing 100 mg of PBB/kg. Interaction between vitamin A deficiency and PBB toxicosis affected vitamin A metabolism as manifested by the appearance of appreciable amounts of retinyl acetate in the liver vitamin A profile. These results suggest an interaction between PBB toxicity and vitamin A and emphasize the importance of nutritional factors such as vitamin A in assessment of PBB toxicosis.