Effects of dietary zinc on free radical generation, lipid peroxidation, and superoxide dismutase in trained mice.

The purpose of this study was to investigate the effects of dietary zinc on free radical generation, lipid peroxidation, and superoxide dismutase (SOD) in exercised mice. In the first part of the study, 48 male weanling mice were randomly divided into three groups. They were fed a zinc-deficient diet containing 1.6 mg/kg zinc or were pair-fed or fed ad libitum a zinc-adequate diet supplemented with 50 mg/kg zinc. Half of each group received an exercise training program that consisted of swimming for 60 min per day in deionized water. The diets and exercise program persisted for 6 weeks. In the second part of the study, 64 mice were fed zinc-deficient diets for 6 weeks, and then one group was fed the zinc-deficient diet for an additional 3 weeks, and the other three groups were fed diets supplemented with 5, 50, and 500 mg/kg zinc, respectively. Half of each group also received the exercise program. Both blood and liver samples were examined. Free radicals in liver were directly detected by electron spin resonance techniques and the extent of lipid peroxidation was indicated by malonic dialdehyde (MDA). Both CuZn-SOD and Mn-SOD were measured. The results showed that exercise training increased the metabolism of zinc, and zinc deficiency induced an increased free radical generation and lipid peroxidation and a decreased hepatic CuZn-SOD activity in exercised mice. Furthermore, although exercise training had no effect on the level of free radicals in zinc-adequate mice, it could increase the hepatic mitochondrial MDA formation further in zinc-deficient animals and zinc deficiency would eliminate the exercise-induced increase in SOD activities which existed in zinc-adequate mice. A total of 50 mg/kg zinc supplemented in the diet was adequate to correct the zinc-deficient status in exercised mice while 5 mg/kg zinc had a satisfactory effect on the recovery of only sedentary zinc-deficient mice. However, 500 mg/kg zinc had a harmful effect on both sedentary and exercised zinc-deficient animals.     

Dietary zinc restriction in rats alters antioxidant status and increases plasma F2 isoprostanes

Approximately 12% of Americans do not consume the estimated average requirement for zinc and could be at risk for zinc deficiency. Since zinc has proposed antioxidant function, inadequate zinc consumption may lead to an enhanced susceptibility to oxidative stress through several mechanisms, including altered antioxidant defenses. In this study, we hypothesized that dietary zinc restriction would result in lower antioxidant status and increased oxidative damage. We fed weanling Sprague-Dawley rats (n=12 per group) a zinc-adequate (50 mg/kg of zinc) diet, a zinc-deficient (<0.05 mg/kg of zinc) diet or a pair-fed diet for 3 weeks and then assessed their antioxidant status and oxidative stress parameters. Rats were zinc deficient as indicated by a significant (P<.05) reduction in body weight (49%) and 19% lower (P<.05) hepatic zinc (20.6+/-2.1 mg/kg) as compared with zinc-adequate rats (24.6+/-2.2 mg/kg). Zinc deficiency resulted in elevated (P<.05) plasma F(2) isoprostanes. Zinc deficiency-mediated oxidative stress was accompanied by a 20% decrease (P<.05) in the ferritin-reducing ability of plasma assay and a 50% reduction in plasma uric acid (P<.05). No significant change in plasma ascorbic acid or in plasma alpha-tocopherol and gamma-tocopherol was observed. However, hepatic alpha-tocopherol and gamma-tocopherol concentrations were decreased by 38% and 27% (P<.05), respectively, as compared with those in zinc-adequate rats. Hepatic alpha-tocopherol transfer protein levels were unaltered (P>.05) by zinc deficiency, but cytochrome P450 (CYP) 4F2 protein levels were elevated (P<.05) as compared with those in zinc-adequate rats. Collectively, zinc deficiency increased oxidative stress, which may be partially explained by increased CYP activity and reductions in hepatic alpha-tocopherol and gamma-tocopherol and in plasma uric acid.     

Effects in chicks of arsenic,arginine, and zinc and their interaction on body weight,plasma uric acid,plasma urea,and kidney arginase activity

The interaction among arsenic, zinc, and arginine was studied in chicks using two fully crossed, three-way, two-by-two-by-two experiments. Arsenic at levels of 0 and 2 μg/g zinc at levels of 2.5 (zinc-deficient) and 25 (zinc-adequate) μg/g, and arginine at levels of 0 and 16 mg/g were supplemented to the diet. After 28 d in both experiments, growth was depressed in chicks fed diets either supplemented with arginine or deficient in zinc. Arsenic deprivation depressed growth of chicks fed diets containing the basal level of arginine and 25 μg supplemental Zn/g. Arsenic deprivation had little or no effect on growth of zinc-deprived chicks fed diets containing the basal level of arginine, or in zinc-deprived or zinc-adequate chicks fed supplemental arginine. Zinc-deficiency elevated urea in plasma and arginase activity in kidney. Those elevations, however, were more marked in arsenic-supplemented than in arsenic-deprived chicks. Also, plasma urea and kidney arginase activity were markedly elevated in chicks fed supplemental arginine; the elevations were more marked in zinc-deficient chicks. These findings support the concept that arsenic has a physiological role, associated with zinc, that can influence arginine metabolism in the chick.     

Zinc deficiency and the activities of lipoprotein lipase in plasma and tissues of rats force-fed diets with coconut oil or fish oil

The present study was performed to investigate the effect of zinc deficiency on the activities of lipoprotein lipase in postheparin serum and tissues of rats fed diets containing either coconut oil or fish oil as dietary fat, using a bifactorial experimental design. To ensure an adequate food intake, all the rats were force-fed by gastric tube. Experimental diets contained either 0.8 mg zinc/kg (zinc-deficient diets) or 40 mg zinc/kg (zinc-adequate diets). The effects of zinc deficiency on the activities of lipoprotein lipase in postheparin serum and postprandial triglyceride concentrations and distribution of apolipoproteins in serum lipoproteins depended on the type of dietary fat. Zinc-deficient rats fed the coconut oil diet exhibited a reduced activity of lipoprotein lipase in postheparin serum and adipose tissue, markedly increased concentrations of triglycerides in serum, and a markedly reduced content of apolipoprotein C in triglyceride-rich lipoproteins and high density lipoproteins compared with zinc-adequate rats fed coconut oil. By contrast, zinc-deficient rats fed the fish oil diet did not exhibit reduced activities of lipoprotein lipase in postheparin serum and adipose tissue and increased concentrations of serum lipids compared with zinc-adequate rats fed the fish oil diet. This study suggests that a reduced activity of lipoprotein lipase might contribute to increased postprandial concentrations of serum triglycerides observed in zinc-deficient animals. However, it also demonstrates that the effects of zinc deficiency on lipoprotein metabolism are influenced by dietary fatty acids.     

Morphofunctional analysis of zinc-accumulating capacity of digestive system organs]

The distribution of zinc and related changes have been studied in zinc--loaded chick pancreas, ileum and liver at the ultrastructural level by sulphide--silver method. White Leghorn chicks fed a high zinc diets (50, 500, 1000, 2000 and 4000 mgZn/kg diet) for 6 weeks, were killed at intervals; portions of their organs were fixed for light and electron microscopy; other samples were analyzed for zinc by AA spectrophotometry. A drastic increase of zinc level in chick pancreas fed 2000 mg Zn/kg diet (as ZnCl2) was associated with acinar cell degeneration. Apoptosis was the predominant form of acinar cell deletion. This study provides support for a previously proposed theory that cell injury stimulates passive zinc accumulation.     

Marginal zinc deficiency increases oxidative DNA damage in the prostate after chronic exercise

Approximately 12% of Americans do not consume the recommended level of zinc and could be at risk for marginal zinc deficiency. Zinc functions in antioxidant defense and DNA repair and could be important for prostate health. We hypothesized that marginal zinc deficiency sensitizes the prostate to oxidative stress and DNA damage. Rats were fed a zinc-adequate (ZA; 30 mg Zn/kg) or marginally zinc-deficient (MZD; 5–6 mg Zn/kg) diet for 6 weeks. MZD increased p53 and PARP expression but no change in 8-hydroxy-2′-deoxyguanosine levels was detected. To examine the susceptibility to exogenous oxidative stress, rats fed a ZA or MZD diet were assigned to exercising (EXE) or sedentary (SED) groups for 9 weeks. MZD or EXE alone did not affect oxidative DNA damage in the prostate; however, combined MZD + EXE increased DNA damage in the dorsolateral lobe. PARP and p53 expression was not further induced with MZD + EXE, suggesting that MZD interferes with DNA repair responses to stress. Finally, the addition of phytase to the MZD diet successfully restored zinc levels in the prostate and decreased DNA damage back to ZA levels. Overall, this study suggests that marginal zinc deficiency sensitizes the prostate to oxidative stress and demonstrates the importance of maintaining optimal zinc nutrition in physically active populations.     

Dietary zinc attenuates renal lead deposition but metallothionein is not directly involved

Chronic lead exposure irreversibly damages the kidneys and may be associated with hypertension and renal insufficiency at sub-clinically toxic levels. Zinc supplementation reduces lead absorption and tissue retention in rodent models but the mechanisms are unknown. Metallothionein (MT) may function in lead detoxification. Our objective was to investigate the effects of marginal zinc (MZ) and supplemental zinc (SZ) intakes on renal lead and zinc accumulation, renal MT immunolocalization and levels. Weanling Sprague Dawley rats were assigned to MZ (8 mg Zn/kg diet), zinc-adequate control (CT; 30 mg Zn/kg), zinc-adequate diet-restricted (DR; 30 mg Zn/kg) or SZ (300 mg Zn/kg) groups, with and without lead acetate-containing drinking water (200 mg Pb/L) for 3 weeks. Kidneys were analyzed for lead and zinc by inductively coupled plasma spectroscopy and MT by immunolocalization and Western blotting. MZ had higher renal lead and lower renal zinc concentrations than CT. SZ was more protective than CT against renal lead accumulation. Renal MT levels reflected dietary intake (SZ ≥ DR ≥ CT ≥ MZ) but lead had no effect on MT staining intensity, distribution, or relative protein amounts. In summary, while SZ lowered renal lead concentration, MT did not appear to function in renal lead accumulation. Future studies should explore alternate mechanisms of renal lead detoxification.     

Serum cation profile of broilers at various stages of exposure to deoxynivalenol

The present experiment was carried out to investigate if levels of serum cations in broilers are modulated differently at various stages of exposure to deoxynivalenol (DON). Male broiler chicks at 7 days of age were fed a basal diet (0.27 mg of DON; 0.01 mg of zearalenone/kg), or either a low DON diet (1.68 mg of DON; 0.15 mg of zearalenone/kg) or a high DON diet (12.21 mg of DON; 1.09 mg of zearalenone/kg) produced using extracts from Fusarium graminearum cultures. Blood samples from the birds were collected during weeks 2, 4, and 5 of exposure. The high DON diet resulted in lower serum calcium levels compared to the basal diet at all the 3 sampling stages, while the low DON diet resulted in lower serum calcium levels only during weeks 2 and 5. Serum potassium levels were reduced under both the DON diets during weeks 2 and 5, while no diet-associated changes were found for serum levels of magnesium, sodium, and zinc. Under the present experimental conditions, the serum levels of calcium were consistently modulated in the broilers exposed to the DON-contaminated diets. The modulation of serum levels of potassium was, however, dependent upon the stage of exposure to DON.     

Effects of dietary pyrroloquinoline quinone disodium on growth performance,carcass yield and antioxidant status of broiler chicks

Pyrroloquinoline quinone (PQQ), a putative essential nutrient and redox modulator in microorganisms, cell and animal models, has been recognized as a growth promoter in rodents. Growth performance, carcass yield and antioxidant status were evaluated on broiler chickens fed different levels of PQQ disodium (PQQ.Na₂). A total of 784 day-old male Arbor Acres (AA) broilers were randomly allotted into seven dietary groups: negative control group (NC) fed a basal diet without virginiamycin (VIR) or PQQ.Na₂; a positive control group (PC) fed a diet with 15 mg of VIR/kg diet; and PQQ.Na₂ groups fed with 0.05, 0.10, 0.20, 0.40 or 0.80 mg PQQ.Na₂/kg diet. Each treatment contained eight replicates with 14 birds each. The feeding trial lasted for 6 weeks. The results showed that chicks fed 0.2 mg PQQ.Na₂/kg diet significantly improved growth performance comparable to those in PC group, and the feed efficiency enhancement effects of dietary PQQ.Na₂ was more apparent in grower phase. Dietary addition of PQQ.Na₂ had the potential to stimulate immune organs development, and low level dietary addition (<0.1 mg/kg) increased plasma lysozyme level. Broilers fed 0.2 mg PQQ.Na₂/kg diet gained more carcasses at day 42, and had lower lipid peroxide malondialdehyde content and higher total antioxidant power in plasma. The results indicated that dietary PQQ.Na₂ (0.2 mg/kg diet) had the potential to act as a growth promoter comparable to antibiotic in broiler chicks.     

Marginal Zinc Deficiency Increases Magnesium Retention and Impairs Calcium Utilization in Rats

An experiment with rats was conducted to determine whether magnesium retention is increased and calcium utilization is altered by a marginal zinc deficiency and whether increased oxidative stress induced by a marginal copper deficiency exacerbated responses to a marginal zinc deficiency. Weanling rats were assigned to six groups of ten with dietary treatment variables of low zinc (5 mg/kg for 2 weeks and 8 mg/kg for 7 weeks), low copper (1.5 mg/kg), adequate zinc (15 mg/kg), and adequate copper (6 mg/kg). Two groups of rats were fed the adequate-zinc diet with low or adequate copper and pair-fed with corresponding rats fed the low-zinc diet. When compared to the pair-fed rats, marginal zinc deficiency significantly decreased the urinary excretion of magnesium and calcium, increased the concentrations of magnesium and calcium in the tibia, increased the concentration of magnesium in the kidney, and increased the urinary excretion of helical peptide (bone breakdown product). Marginal copper deficiency decreased extracellular superoxide dismutase and glutathione, which suggests increased oxidative stress. None of the variables responding to the marginal zinc deficiency were significantly altered by the marginal copper deficiency. The findings in the present experiment suggest that increased magnesium retention and impaired calcium utilization are indicators of marginal zinc deficiency. Mention of a trademark or proprietary product does not constitute a guarantee or warranty by the U.S. Department of Agriculture and does not imply its approval to the exclusion of other products that also might be suitable. The U.S. Department of Agriculture, Agricultural Research Service, Northern Plains Area is an equal opportunity/affirmative action employer, and all agency services are available without discrimination.     

Zinc-deficient rats have more limited bone recovery during repletion than diet-restricted rats

The objective of this study was to investigate the effects of dietary zinc deficiency and diet restriction on bone development in growing rats, and to determine whether any adverse effects could be reversed by dietary repletion. Weanling rats were fed either a zinc-deficient diet ad libitum (ZD; <1 mg zinc/kg) or nutritionally complete diet (30 mg zinc/kg) either ad libitum (CTL) or pair-fed to the intake of the ZD group (DR; diet-restricted) for 3 weeks (deficiency phase) and then all groups were fed the zinc-adequate diet ad libitum for 3, 7, or 23 days (repletion phase). Excised femurs were analyzed for bone mineral density (BMD) using dual-energy x-ray absorptiometry, and plasma was analyzed for markers of bone formation (osteocalcin) and resorption (Ratlaps). After the deficiency phase, ZD had lower body weight and reduced femur BMD, zinc, and phosphorus concentrations compared with DR; and these parameters were lower in DR compared with CTL. Femur calcium concentrations were unchanged among the groups. Reduced plasma osteocalcin in ZD and elevated plasma Ratlaps in DR suggested that zinc deficiency limits bone formation while diet restriction accelerates bone resorption activity. After 23 days of repletion, femur size, BMD, and zinc concentrations remained lower in ZD compared with DR and CTL. Body weight and femur phosphorus concentrations remained lower in both ZD and DR compared with CTL after repletion. There were no differences in plasma osteocalcin concentrations after the repletion phase, but the plasma Ratlaps concentrations remained elevated in DR compared with CTL. In summary, both ZD and DR lead to osteopenia during rapid growth, but the mechanisms appear to be due to reduced modeling in ZD and higher turnover in DR. Zinc deficiency was associated with a greater impairment in bone development than diet restriction, and both deficiencies limited bone recovery during repletion in growing rats.     

Bioavailability of two organic forms of zinc in comparison to zinc sulphate for weaning pigs fed a diet composed mainly of wheat, barley and soybean meal

This study was performed to compare the bioavailability of two organic zinc compounds, a zinc glycinate complex and a zinc amino acid chelate with that of zinc sulphate in growing pigs fed a basal diet composed mainly of wheat, barley and soybean meal. The experiment included 96 pigs with an average body weight of 8 kg, allotted to ten groups of nine to ten pigs each. The first group received the basal diet, containing 42 mg of native zinc per kg, without zinc supplementation over a period of five weeks. The other nine groups received the basal diet supplemented with 15, 30 or 50 mg of zinc/kg as zinc sulphate, zinc glycinate or the zinc amino acid chelate. Pigs fed the unsupplemented diet had a lower growth performance (body weight gain, feed conversion ratio) than the other nine groups. Supplementation of 15 mg zinc/kg diet (irrespective of zinc form) was sufficient to yield optimum growth performance. Plasma zinc concentration and activity of alkaline phosphatase were rising with increasing zinc supplementation levels up to a maximum reached at a supplementary level of 30 or 50 mg/kg diet for activity of alkaline phosphatase and plasma zinc concentration, respectively. The response of those parameters to zinc supplementation did, however, not differ between the three zinc compounds considered. The apparent digestibility of zinc from the diet was also not different for the three zinc compounds. In conclusion, these findings show that the bioavailability of the two organic zinc compounds did not differ from that of zinc sulphate in growing pigs fed a diet with wheat, barley and soybean meal as major components.     

Selenium Supplementation Modulates Zinc Levels and Antioxidant Values in Blood and Tissues of Diabetic Rats Fed Zinc-Deficient Diet

Diabetes mellitus is associated to a reduction of antioxidant defenses that leads to oxidative stress and complications in diabetic individuals. The present study was undertaken to investigate the effect of selenium on blood biochemical parameters, antioxidant enzyme activities, and tissue zinc levels in alloxan-induced diabetic rats fed a zinc-deficient diet. The rats were divided into two groups; the first group was fed a zinc-sufficient diet, while the second group was fed a zinc-deficient diet. Half of each group was treated orally with 0.5 mg/kg sodium selenite. Tissue and blood samples were taken from all animals after 28 days of treatment. At the end of the experiment, the body weight gain and food intake of the zinc-deficient diabetic animals were lower than that of zinc-adequate diabetic animals. Inadequate dietary zinc intake increased glucose, lipids, triglycerides, urea, and liver lipid peroxidation levels. In contrast, serum protein, reduced glutathione, plasma zinc and tissue levels were decreased. A zinc-deficient diet led also to an increase in serum glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, and liver glutathione-S-transferase and to a decrease in serum alkaline phosphatase activity and glutathione peroxidase. Selenium treatment ameliorated all the values approximately to their normal levels. In conclusion, selenium supplementation presumably acting as an antioxidant led to an improvement of insulin activity, significantly reducing the severity of zinc deficiency in diabetes.     

Bioavailability of two organic forms of zinc in comparison to zinc sulphate for weaning pigs fed a diet composed mainly of wheat,barley and soybean meal

This study was performed to compare the bioavailability of two organic zinc compounds, a zinc glycinate complex and a zinc amino acid chelate with that of zinc sulphate in growing pigs fed a basal diet composed mainly of wheat, barley and soybean meal. The experiment included 96 pigs with an average body weight of 8 kg, allotted to ten groups of nine to ten pigs each. The first group received the basal diet, containing 42 mg of native zinc per kg, without zinc supplementation over a period of five weeks. The other nine groups received the basal diet supplemented with 15, 30 or 50 mg of zinc/kg as zinc sulphate, zinc glycinate or the zinc amino acid chelate. Pigs fed the unsupplemented diet had a lower growth performance (body weight gain, feed conversion ratio) than the other nine groups. Supplementation of 15 mg zinc/kg diet (irrespective of zinc form) was sufficient to yield optimum growth performance. Plasma zinc concentration and activity of alkaline phosphatase were rising with increasing zinc supplementation levels up toa maximum reached at a supplementary level of 30 or 50 mg/kg diet for activity of alkaline phosphatase and plasma zinc concentration, respectively. The response of those parameters to zinc supplementation did, however, not differ between thethree zinc compounds considered. The apparent digestibility of zinc from the diet was also not different for the three zinc compounds. In conclusion, these findings show that the bioavailability of the two organic zinc compounds did not differ from that of zinc sulphate in growing pigs fed a diet with wheat, barley and soybean meal as major components.     

Effects of dietary zinc and copper on free radical production in rat lung and liver

The effects of dietary copper and zinc on free radical production in lung and liver microsomes were studied in male weanling rats. The rats were fed for 6 weeks on one of seven diets, with different copper and zinc concentrations representing low, adequate, and high dietary levels of copper and low and adequate levels of zinc. Rats were put on diets arranged in a 3 X 2 factorial design with copper and zinc supplementations of 0, 15, and 500 mg/kg and 0.5 or 100 mg/kg, respectively. The low copper diet depressed copper levels in both the lungs and liver, although zinc levels were unchanged in rats on the low zinc diets. Endogenous carbon-centered lipid radical production in microsomes induced by NADPH was measured using spin-trapping techniques. The low zinc diets increased free radical production in lung microsomes but not in liver microsomes. No change in free radical production was observed in lung or liver microsomes obtained from rats on low copper diets. The data indicate that endogenous free radical production is increased in lung microsomes as a function of dietary zinc deficiency but is not influenced by copper status.     

Effects of chronic lead and cadmium exposure on blood pressure in occupationally exposed workers

Studies were carried out to determine the effect of dietary vanadium on chicks fed phosphorus deficient and control diets. Vanadium at 50 mg/kg of diet decreased growth of both control and deficient chicks. The high mortality among the phosphorus deficient chicks was significantly alleviated by the presence of vanadium. The increased relative ventricular weights found among the deficient chicks was also alleviated by the presence of dietary vanadium. Vanadium fed at 10 or 20 mg/kg diet did not reduce growth rate but significantly reduced mortality among chicks fed the deficient diet and decreased the relative ventricle weights. Time course studies revealed that chicks are hatched with high relative ventricular weights (.83% of body wt) and remain at that level among chicks fed the phosphorus deficient diet. The addition of vanadium or phosphate to the diet resulted in a progressive decrease in relative ventricular weights. The inclusion of vanadium in the diet resulted in increased serum phosphorus levels among the deficient chicks that may be related to the decrease in mortality and relative ventricle weights.     

The effects of betamethasone, low calcium and low phosphorus diets on growth in chicks

The effects of oral betamethasone (25 micrograms/kg/d), low calcium (1 g/kg), and low phosphorus (2,5 g/kg) diets on weight gain were investigated in 513 growing chicks. The chicks were divided according to initial weight into a lower weight group (less than 100 g each) and a higher group (more than 100 g each). The increases in weight were recorded after periods of 7, 14 and 21 days. The increases in weight in the older chicks (high weight group) were less than in the younger chicks. There was a greater reduction in rate of growth in chicks fed the low phosphorus diet than in those fed the low calcium diet, particularly in the older birds. Betamethasone administration also reduced the rate of growth but this was not additive to the effect of a low calcium diet. In contrast, the greatest reduction in growth rate was observed in the chicks fed the low phosphorus diet and given betamethasone.     

Low zinc intake decreases the lymphatic output of retinol in rats infused intraduodenally with beta-carotene

Previously, we have shown that the lymphatic absorption of retinol is significantly decreased in rats fed a low zinc diet. This study was conducted to determine whether the absorption of beta-carotene also is altered in zinc-deficient male rats. The absorption of beta-carotene was estimated by determining the amount of retinol appearing in the mesenteric lymph during intraduodenal infusion of beta-carotene. One group of rats was fed the AIN-93G diet but low in zinc (LZ; 3 mg/kg) and the other was fed the same diet adequate in zinc (AZ; 30 mg/kg). The LZ and AZ rats were trained to meal feed equal amounts of the diets twice daily. At 6 weeks, each rat with lymph cannula was infused via an intraduodenal catheter at 3 ml/h for 8 h with a lipid emulsion containing 65.0 nM beta-carotene, 565.1 microM triolein, 27.8 kBq 14C-triolein (14C-OA), 72 mg albumin, and 396 microM Na-taurocholate in 24 ml PBS (pH 6.7). The lymphatic output of retinol over the 8-h period was significantly lower in LZ rats than in AZ rats. The absorption of 14C-OA also was significantly lower in LZ rats. No significant differences were observed between groups in intestinal beta-carotene 15,15'-dioxygenase, retinal reductase, and retinal oxidase activities. The findings demonstrate that low zinc intake or marginal zinc deficiency significantly lowers the absorption of beta-carotene as estimated by lymphatic retinol output. The results also indicate that the decrease in retinol output in LZ rats is not linked to defects in beta-carotene cleavage and subsequent conversion of retinal to retinol in the intestinal mucosa. This study suggests that zinc status is an important factor determining the intestinal absorption of beta-carotene and hence the nutritional status of vitamin A.