Effects Of Zn Deficiency Research Articles

Pathology of the thymus, spleen and bursa of Fabricius in zinc-deficient ducklings

The weight and growth index of bursa of Fabricius, thymus and spleen were significantly reduced (P < 0.05 or P < 0.01) in zinc (Zn)-deficient ducks (Zn 22.9 mglkg diet) when compared with normal ducks. The G0/Gl phase of the cell cycle of the bursa of Fabricius, thymus and spleen was much higher, and the S and G2+M phases lower in Zn-deficient ducks than in the controls. Histopathologically, there was lymphocyte degeneration and depletion of lymphoid organs, and the reticular cells of thymus were also degenerate or necrotic in the Zndeficient group. The results demonstrated that Zn deficiency seriously inhibited the growth of lymphoid organs and caused marked pathology in the lymphoid organs. The results also showed that the effect of Zn deficiency on the primary lymphoid organs occurred earlier than on the secondary lymphoid organs. The effect of Zn deficiency was greatest on the bursa of Fabricius, followed by the thymus, and then the spleen.

Influence of Gyttja on Shoot Growth and Shoot Concentrations of Zinc and Boron of Wheat Cultivars Grown on Zinc‐Deficient and Boron‐Toxic Soil

Greenhouse experiments were carried out to study the influence of gyttja, a sedimentary peat, on the shoot dry weight and shoot concentrations of zinc (Zn) and boron (B) in one bread wheat (Triticum aestivum L., cv. Bezostaja) and one durum wheat (Triticum durum L., cv. Kiziltan) cultivar. Plants were grown in a Zn‐deficient (DTPA‐Zn: 0.09 mg kg−1 soil) and B‐toxic soil (CaCl2/mannitol‐extractable B: 10.5 mg kg−1 soil) with (+Zn = 5 mg Zn kg−1 soil) and without (−Zn = 0) Zn supply for 55 days. Gyttja containing 545 g kg−1 organic matter was applied to the soil at the rates of 0, 1, 2.5, 5, and 10% (w/w). When Zn and gyttja were not added, plants showed leaf symptoms of Zn deficiency and B toxicity, and had a reduced growth. With increased rates of gyttja application, shoot growth of both cultivars was significantly enhanced under Zn deficiency, but not at sufficient supply of Zn. The adverse effects of Zn deficiency and B toxicity on shoot dry matter production became very minimal at the highest rate of gyttja application. Increases in gyttja application significantly enhanced shoot concentrations of Zn in plants grown without addition of inorganic Zn. In Zn‐sufficient plants, the gyttja application up to 5% (w/w) did not affect Zn concentration in shoots, but at the highest rate of gyttja application there was a clear decrease in shoot Zn concentration. Irrespective of Zn supply, the gyttja application strongly decreased shoot concentration of B in plants, particularly in durum wheat. For example, in Zn‐deficient Kiziltan shoot concentration of B was reduced from 385 mg kg−1 to 214 mg kg−1 with an increased gyttja application. The results obtained indicate that gyttja is a useful organic material improving Zn nutrition of plants in Zn‐deficient soils and alleviating adverse effects of B toxicity on plant growth. The beneficial effects of gyttja on plant growth in the Zn‐deficient and B‐toxic soil were discussed in terms of increases in plant available concentration of Zn in soil and reduction of B uptake due to formation of tightly bound complexes of B with gyttja.

CHRONIC ZINC DEFICIENCY INDUCES AN ANTIOXIDANT ADAPTIVE RESPONSE IN RAT LUNG

Few studies are available about the role of dietary zinc (Zn) in respiratory diseases. Adult male rats were divided into 2 groups and fed respectively a moderate Zn-deficient diet and a Zn-adequate control diet. In lung tissue at 2 months, thiobarbituric acid-reactive species (TBARS), total glutathione, glutathione disulfide, protein carbonyls, metallothionein, and the activities of glutathione peroxidase (GPx), catalase, CuZn-superoxide dismutase (CuZnSOD) and glucose-6-phosphate dehydrogenase (G-6-PDH) were increased, but protein thiols decreased. In lung tissue at 4 months, TBARS, metallothionein, and the activities of CuZnSOD, Mn-superoxide dismutase (MnSOD) increased. The activities GPx, catalase, G-6-PDH were lower than control group. The changes were accompanied by histological alterations in Zn-deficient lung. The results provide evidence of the pro-oxidative effects of Zn-deficiency in lung, and suggest that the time of treatment play a key role in determining lung susceptibility to oxidative stress.

Effect of Zn deficiency and subsequent Zn repletion on bone mineral composition and markers of bone tissue metabolism in 65Zn-labelled, young-adult rats.

The objective of the present study was to investigate the effect of changing skeletal Zn load (mobilization/restoring) on bone mineral composition and bone tissue metabolism. For this purpose, 36 65Zn-labelled, young-adult female rats were fed with either a purified diet with sufficient Zn (21 microg/g, control) for 26 days, or deficient Zn (1.4 microg/g) for 12 days followed by 14 days repletion with the control diet. The animals were killed at the onset of the study (reference: n=4), at the end of the Zn deficiency episode (control: n=4; Zn deficiency: n=4), subgroups (n=4) of Zn repleted animals at repletion days 2, 4, 7, 10 and 14, and at day 14 the remaining controls also (n=4). Zn deficiency reduced skeletal Zn concentration from 198 to 155 microg/g of bone dry matter. About half of mobilized skeletal Zn was refilled within 2 days of repletion and was completely restored until the end of the study. Concentrations of bone ash, Ca, P and Mg remained constant (means in bone dry matter: 51% bone ash, 191 mg Ca/g, 95 mg P/g, 4.4 mg Mg/g). Blood plasma concentrations of osteocalcin and daily urinary excretions of pyridinoline PYD and dexoxypyridinoline DPD were unaffected by treatment (mean: 57 ng/ml, 222 nmol/day, 137 nmol/day). Also daily urinary excretions of Ca, P and Mg remained fairly constant (means: 0.26 mg/day, 16 mg/day, 1.5 mg/day). 65Zn autoradiography of femur sections revealed a pronounced Zn exchange in the area of the metaphysis and epiphysis. We conclude that transient mobilization and restoration of skeletal Zn occurs mainly in trabecular bone, and does not involve major changes in bone mass, macro mineral content, or bone tissue turnover in young-adult rats.

Effect of marginal zinc deficiency on human growth and development.

Growth and development disorders in humans caused by zinc (Zn) deficiency have been investigated for a long time. Although marginal Zn deficiency is a common nutritional problem around the world, especially in the children of developing countries where diets have less Zn available, it is difficult to identify. This review provides the progression of studies in the effect of Zn deficiency on human growth and development, and also explains the possible mechanisms of how Zn promotes these phenomena. These mechanisms involve the effects of Zn on DNA synthesis, RNA synthesis, and cell division. The concept of zn-finger proteins explains the role of Zn in gene expression and endocrine function. Findings indicate that Zn deficiency can result in delayed growth and development which can be corrected in part by Zn supplementation.

Effect of Zn deficiency on net photosynthetic rate, 14C partitioning, and oil accumulation in leaves of peppermint

Changes in growth, CO2 exchange rate, and distribution of photosynthetically fixed 14CO2 into the primary photosynthetic metabolic pool (sugars, amino acids and organic acids) and essential oil accumulation were determined in leaves (leaf positions 1-6 from apex) of developing peppermint grown in a solution culture at Zn concentrations of 0 and 0.05 g m-3. There was a significant decrease in 14C incorporation in total, ethanol-soluble and ethanol-insoluble fractions in Zn deficient plants at all leaf positions. 14C incorporated in essential oil and in sugars were significantly higher in leaf pairs 1 to 3 than in leaf pairs 4 to 6. 14C incorporation into amino acids and organic acids was higher in all leaf pairs in Zn deficient plants. Statistical analysis showed a positive significant association between Zn content of leaf and 14C incorporation into ethanol-soluble fraction and sugars and a negative correlation with 14C incorporation into amino acids and organic acids. Hence the content of sugars in leaves significantly influences essential oil accumulation under Zn stress.

Responses of Six Crop Species to Solution Zinc2+ Activities Buffered with HEDTA

AbstractZinc contamination has long hampered the use of conventional nutrient solutions for attaining reproducible and severe Zn deficiencies. Chelator‐buffered solutions show promise for precisely imposing micronutrient deficiencies, but further studies are needed to fully evaluate the method and to develop methods to avoid Zn‐deficiency‐induced P toxicity. In a greenhouse study, seedlings of maize (Zea mays L. ‘Golden Cross Bantam’), wheat (Triticum aestivum L. ‘Yecora Rojo’), tall wheatgrass (Elytrigia pontica [Podp.] Holub ‘Orbit’), alfalfa (Medicago sativa L. ‘Germain's WL‐320’), soybean (Glycine max [L.] Merr. ‘Vinton 81’), and tomato (Lycopersicon esculentum L. ‘Jackpot’) were grown for 16 to 29 d in solutions containing 0.4 to 12 µM total Zn. Computed Zn2+ activities were buffered at 4 to 123 pmol L−1 by a 50‐µM excess of HEDTA, and solution P was maintained at 10 ± 3 µM. Zinc deficiencies ranged from mild to severe, dry matter yield minima ranged from 32 to 89% of controls, and critical Zn2+ activities for the onset of deficiency ranged from approximately 10 to 65 pmol L−1. The relative sensitivity of the six species to low Zn was maize &gt; tomato &gt; wheat &gt; alfalfa ≈ tall wheatgrass &gt; soybean. Shoot Zn concentrations were consistent with the widely reported critical range of 15 to 20 mg kg−1. Zinc deficiency in the three grass species led to hyperaccumulation of P to phytotoxic levels, and leaf symptoms largely reflected this toxicity. Leaf P concentrations in the three dicots tended to be lower, but may have been within the phytotoxic range. Thus, even with P concentrations that approach soil solution values, the P toxicity that often accompanies Zn deficiency in solution‐culture experiments was not eliminated. The effects of Zn deficiency on shoot concentrations of nutrients other than P were variable, although divalent cations tended to be elevated in Zn‐deficient shoots.

Effect of Marginal Zinc Deficiency on Human Growth and Development

Growth and development disorders in humans caused by zinc (Zn) deficiency have been investigated for a long time. Although marginal Zn deficiency is a common nutritional problem around the world, especially in the children of developing countries where diets have less Zn available, it is difficult to identify. This review provides the progression of studies in the effect of Zn deficiency on human growth and development, and also explains the possible mechanisms of how Zn promotes these phenomena. These mechanisms involve the effects of Zn on DNA synthesis, RNA synthesis, and cell division. The concept of Zn-finger proteins explains the role of Zn in gene expression and endocrine function. Findings indicate that Zn deficiency can result in delayed growth and development which can be corrected in part by Zn supplementation.

Zinc deficiency affects the activity and protein concentration of angiotensin-converting enzyme in rat testes.

Zinc (Zn) deficiency causes hypogonadism in a number of different species. Previous work has shown that Zn deficiency reduces the activity of angiotensin-converting enzyme (ACE), a Zn-dependent enzyme, in the testes of prepubertal rats. These studies were designed to determine whether this effect was caused by a change in the concentration of ACE protein. Thirty-five male rats at 26 days of age were divided into three groups. One group was fed ad libitum a Zn-adequate diet (40 mg/kg); another group was fed a similar diet, but deficient in Zn (< 1.0 mg/kg); a third group was pair-fed to the deficient group. After 4 weeks on these regimens, all rats in the ad libitum-fed group and half of the rats in each of the deficient and pair-fed groups were sacrificed, and tissues were collected for analysis. The remaining animals in the Zn-deficient and pair-fed groups were fed a Zn-adequate diet ad libitum for another 2 weeks, then sacrificed. With the use of an enzyme-linked immunosorbent assay for testicular ACE protein, the effect of these treatments on the concentration of ACE protein in testes was determined. After 4 weeks, ACE activity in testes of the Zn-deficient rats was reduced by 74% compared to that in the ad libitum-fed controls. This was accompanied by a 64% reduction in the amount of ACE protein in the testes. There was not a significant effect of pair-feeding. Refeeding Zn-deficient rats a Zn-adequate diet for 2 weeks restored ACE protein concentrations and ACE activity to values not significantly different from those in pair-fed controls. Soluble ACE, but not particulate ACE, of the epididymis was significantly reduced by Zn deficiency. Because the ACE activity of testes has been found primarily in the germinal cells, and soluble ACE in the epididymis is derived from the testes, these findings suggest that the effects of Zn deficiency on testicular and epididymal ACE is caused by an impairment of spermatid development.

Reproductive Pecan

The effect of Zn deficiency on reproductive growth of `Stuart' pecan [Carya illinoensis (Wangenh.) C. Koch] was studied. At the most severe Zn-deficiency level, shoots were rosetted and produced neither. staminate nor pistillate inflorescences. At less severe Zn-deficiency levels, catkin length and weight decreased as Zn concentration in the leaf decreased. The number of fruits produced per shoot was reduced by Zn deficiency. Even though fruit abortion was not affected by Zn status of the shoot, fruit death and drying in situ increased with increasing Zn deficiency. Zinc deficiency dramatically suppressed fruit development and resulted in delayed and staggered shuck dehiscence.

Effect of zinc deficiency in wheat on the release of zinc and iron mobilizing root exudates

AbstractThe effect of Zn deficiency in wheat (Triticum aestivum L. cv. Ares) on the release of Zn mobilizing root exudates was studied in nutrient solution. Compared to Zn sufficient plants, Zn deficient plants had higher root and lower shoot dry weights. After visual Zn deficiency symptoms in leaves appeared (15–17 day old plants) there was a severalfold increase in the release of root exudates efficient at mobilizing Zn from either a selective cation exchanger (Zn‐chelite) or a calcareous soil. The release of these root exudates by Zn deficient plants followed a distinct diurnal rhythm with a maximum between 2 and 8 h after the onset of light. Re‐supply of Zn to deficient plants depressed the release of Zn mobilizing root exudates within 12 h to about 50%‐, and after 72 h to the level of the control plants (Zn sufficient plants).The root exudates of Zn deficient wheat plants were equally effective at mobilizing Fe from freshly precipitated FeIII hydroxide as Zn from Zn‐chelite. Furthermore, root exudates from Fe deficient wheat plants mobilized Zn from Zn‐chelite, as well as Fe from FeIII hydroxide. Purification of the root exudates and identification by HPLC indicated that under Zn as well as under Fe deficiency, wheat roots of the cv. Ares released the phytosiderophore 2′‐deoxymugineic acid. Additional experiments with barley (Hordeum vulgare L. cv. Europa) showed that in this species another phytosiderophore (epi‐3‐hydroxymugineic acid) was released under both Zn and Fe deficiencies.These results demonstrate that the enhanced release of phytosiderophores by roots of grasses is not a response mechanism specific for Fe deficiency, but also occurs under Zn deficiency. The ecological relevance of enhanced release of phytosiderophore also under Zn deficiency is discussed.

Evidence that adverse effects of zinc deficiency on essential fatty acid composition in rats are independent of food intake.

1. Young male rats were fed on diets containing 3.4, 36 or 411 mg zinc/kg for 10 weeks in order to determine whether effects of Zn deficiency on plasma and liver essential fatty acid composition could be distinguished from those of reduced protein and energy intake. 2. Fatty acid analysis revealed that a Zn intake of 3.4 mg/kg (plasma Zn 0.80 v. 1.97 mmol/l in controls fed on 36 mg Zn/kg) resulted in a significant increase in the linoleic acid:arachidonic acid ratio in both plasma and liver phospholipids in comparison with rats fed on 36 or 411 mg Zn/kg. 3. Zn supplementation (411 mg/kg) decreased the linoleic acid:arachidonic acid ratio in plasma phosphatidylserine compared with that of the controls. 4. The previously reported increase in arachidonic acid (mol %) in liver triacylglycerol of Zn-deficient rats was shown to be a function of a reduced liver triacylglycerol pool size; quantitatively, triacylglycerol content of arachidonic acid in the liver was not significantly affected by Zn intake.

Effects of Zn deficiency on thymus of growing rats

Zinc (Zn) deficiency is thought to cause depressed immune function in both the cell mediated and humoral aspects of the system. Alteration of lymphocyte maturation and migration has been observed in Zn-deficiency and marked reduction of the lymphocyte number was noted in the thymus of the pups fed Zn-deficient diet. Other alterations include parakeratosis of the squamous epithelia of digestive system and skin.Three groups of seven, weanling, male Wistar rats each were fed diets containing either 1.1 ppm Zn (deficient) or supplemented with 100 ppm Zn ad libitum (control) or the Zn supplemented diet limited to the amount consumed by those on the deficient diet (pair-fed) for 3 weeks. Details of the diet compositions have been reported previously (7). The animals were weighed at the onset and end of the experiment. The organ was weighed after it was fixed in Karnovsky's fixative and small pieces of the tissue were post-fixed in 2.0%, OsO4 for electron microscopy.

Micronutrients

Four crops, corn, pearl‐millet, sorghum, and cowpea were evaluated for their relative Zn response at 0 (original Zn deficient soil), 1, 2, 3, 4, 5, 10, 20, 40 and 100 mg Zn kg‐1 soil under greenhouse conditions. Corn and pearl‐millet were harvested at earing, and sorghum and cowpea at maturity. Crops differed in their response to Zn deficiency in soil. Zinc deficiency symptoms were more severe in corn and cowpea than sorghum and pearl‐millet. The maximum yields in corn, pearl‐millet, sorghum‐stover, sorghum‐grain, cowpea‐straw and cowpea‐grain were recorded at 4, 4, 1, 5, 2, and 5 mg Zn kg‐1 soil, respectively, which were 5628, 191, 86, 563, 304 and 723% more than at 0 Zn. Adverse effects of Zn deficiency were more pronounced on grain yield of sorghum and cowpea than their stover/straw components. Zinc, more than 20 mg kg‐1 soil, caused depressed pearl‐millet and cowpea yields. In corn and cowpea, showing severe Zn deficiency symptoms, shoot Zn at 0 Zn was more than plants receiving 10 and 2 mg Z...

Effect of Zn deficiency on serum vitamin A level, tissue enzymes and histological alterations in goats

An experiment was conducted to elucidate the effect of dietary zinc on serum vitamin A levels and its influence on certain enzyme activities in ovaries using 16 female kids, divided into four groups. The animals in group 1 and 2 were fed a basal diet (15 p.p.m. zinc) whereas those in groups 3 and 4 were supplemented with 65 p.p.m. zinc. Groups 2 and 4 were supplemented with 1800 i.u. of vitamin A kg diet. The development of deficiency symptoms in a few animals after a period of 46–177 days was taken as an index to kill the animals periodically for collection of tissues. The mean zinc levels were significantly ( P < 0.01) higher in zinc-supplemented groups compared to controls. The zinc supplementation resulted in significantly higher levels of serum vitamin A in group 4 compared to those in other groups ( P < 0.01). The alcohol dehydrogenase activity in liver, intestine and retina was significantly greater ( P < 0.01) in groups 3 and 4 than in zinc-deficient groups. In liver ( P < 0.01) and ovaries ( P < 0.05) of zinc-supplemented animals, the superoxide dismutase activity was higher. The microsections of ovary from the animals of groups 1 and 2 showed deformed ateretic follicles, whereas in group 3 some deformed ova were seen. However, the animals in group 4 did not show any such abnormality, indicating that zinc and vitamin A were both necessary for the normal functioning of the germinal epithelium of the ovary.

The effect of zinc deficiency on glucose metabolism in meal-fed rats.

The incorporation of uniformly-labelled [14C]glucose into fatty acids and glycogen of adipose tissue and liver was used to assess the effects of zinc deficiency on glucose metabolism in meal-fed rats. Throughout the study, identical feeding regimens were maintained between each of the Zn-deficient groups and their appropriate controls. The feeding regimens were either meal-feeding or ad lib. feeding. Zn deficiency reduced [14C]glucose incorporation into fatty acids of epididymal fat pads of meal-fed rats by 75% when compared with meal-fed controls. Zn deficiency caused a slight but significant decrease in [14C]glucose incorporation into liver fatty acids of meal-fed fats when compared with meal-fed controls. Zn deficiency significantly increased [14C]glucose incorporation into liver glycogen of meal-fed rats in Expt. 2 but not in Expt 1. Some effects of Zn deficiency on glucose metabolism were shown to be independent of the feeding regimen when a single daily meal was given to both Zn deficient and control groups. This method of feeding may be a useful approach to study the effects of Zn on glucose metabolism in the rat.

Studies on photosynthetic electron transport, photophosphorylation and CO2fixation in zinc deficient leaf cells ofZea mavs. L.

Abstract The effect of Zn deficiency on rate of photosynthesis of leaf discs, isolated mesophyll and bundle sheath cells and chloroplasts of maize (Zea mays. L) was studied. The yield of mesophyll and bundle sheath cells obtained by enzymic digestion of the leaf tissues from Zn deficient plants is lower than the identical tissues from normal plants which suggests that Zn deficiency brings about some structural changes in the leaf cell. Photosynthetic oxygen evolution measured in the leaf discs is low due to Zn deficiency. Photosystem‐II dependent Hill reaction and non cyclic photophosphorylation of chloroplasts were also affected by Zn deficiency. Rate of photosynthetic carbon dioxide fixation by both bundle sheath and mesophyll cells obtained from Zn deficient leaf‐tissue waslower than the cells free from Zn deficiency. Addition of various metabolites like NADPH, ATP and PEP to Zn deficient mesophyll cells whowed marked enhancement in 14‐CO2 fixation. However, addition of NADPH, ATP and RuBP to Zn defici...

Effect of zinc deficiency on the weight, cellularity and zinc concentration of different skeletal muscles in the post-weanling rat.

Zinc-deficient (ZD), weight-restricted (WR), pair-fed (PF) andad lib.-fed (AL) Sprague-Dawley male rats were killed after feeding the respective Zn-deficient and Zn-supplemented diets from 3 to 8 weeks of age. Animals killed at the start of the experiment served as a baseline control (BC).Four different skeletal muscles – biceps brachii, soleus, plantaris and extensor digitorum longus (EDL) – were studied for changes in weight, the number and diameter of muscle fibres and Zn concentration.The soleus muscle had the highest concentration of Zn. It was the only muscle to reduce its Zn concentration due to Zn deficiency.There was a loss of muscle fibres during normal growth (groups BCv.AL) in the soleus muscle (P&lt; 0.05). The estimated length of muscle and the diameter of the muscle fibres in all four muscles increased significantly (P&lt; 0.001). Therefore postweanling growth appears to occur as a result of longitudinal and transverse increases in the dimensions of these muscles.The reduction in muscle fibre number in ZD rats compared to BC animals may occur within the range of expected fibre loss during normal growth. Fibre loss in ZD rats may be more affected by feeding-pattern-dependent metabolic changes than by a deficiency of Zn per se (groups ZDv.WR). Soleus fibre loss in ZD rats may be related to the high Zn concentration in this muscle.The effect of Zn deficiency per se on muscle fibre diameter may be inaccurately interpreted by comparing the ZD animals with their PF and AL controls. There was no significant difference in fibre diameter in any of the four muscles when ZD and WF rats were compared.

Response of Submandibular Gland of the Rat to Nutritional Zinc Deficiency

Studies in several laboratories have shown that nutritional Zn deficiency in the rat causes a reduction in the activity of certain Zn-dependent enzymes in kidney, intestine, pancreas, etc. The present report deals with the effects of Zn-deficiency on submandibular gland of the rat. For the sake of comparison with previous studies, some assays on pancreas were included. Protein content, DNA, acid phosphatase, and acid protease activities were not affected in submandibular gland. Lactate dehydrogenase was unaffected in submandibular gland and showed increased activity in pancreas. Malate dehydrogenase was significantly decreased in both organs, the decrease being more marked in submandibular gland. Alkaline phosphatase activity in submandibular glands of control rats was about 10-fold higher than in pancreas. In the zinc-deficient rats, alkaline phosphatase was reduced to 59% of controls in the submandibular glands and to about 75% in pancreas. It is known from histochemical studies that in the submandibular gland this enzyme is confined to the myoepithelial cells. Recent studies attribute to salivary glands a role in the etiology of taste disturbances seen in clinical states of zinc deficiency. It is proposed that functional impairment of the myoepithelial cells might contribute to the disturbance of taste.

Effect of age, weight and adequacy of zinc intake on the balance between alkaline ribonuclease and ribonuclease inhibitor in various tissues of the rat

1. Deficiency of zinc inhibits growth and also increases the activity of alkaline ribonuclease in certain tissues of the rat (Prasad & Oberleas, 1973). Zn could influence ribonuclease activity by direct effects on the enzyme or its natural inhibitor, or non-specifically as occurs when growth rate is affected by various other factors. These possibilities were studied. 2. Alkaline ribonuclease was shown to be inhibited by Zn in vitro, but the concentrations of Zn required were so high that the enzyme was probably not directly affected by changes in tissue Zn concentration caused by dietary deficiency. 3. At lower concentrations, Zn added in vitro increased the activity of alkaline ribonuclease in tissue homogenates probably by inactivating the inhibitor of the enzyme. 4. Age, weight and particularly food restriction caused tissue-specific alterations of ribonuclease and ribonuclease inhibitor concentrations in liver, kidney, oesophagus, testis and thymus. 5. The ribonuclease activities in liver, kidney and testis of Zn-deficient rats were unaltered in comparison with those of pair-fed rats. In thymus, which decreased in weight in the Zn-deficient animals, there was a concomitant increase in ribonuclease activity, but in oesophagus, the deficiency reduced the activity of ribonuclease. 6. The effects of Zn deficiency upon alkaline ribonuclease and its inhibitor are probably secondary consequences of reductions in food intake or growth.