Oral Administration Of Zinc Sulfate Research Articles

Oral Administration of Zinc Sulfate with Intramuscular Foot-and-Mouth Disease Vaccine Enhances Mucosal and Systemic Immunity

Background/Objectives: Foot-and-mouth disease (FMD) remains a significant global threat to livestock farming. Current commercial FMD vaccines present several challenges, including the risk of infection and adverse injection site reactions due to oil-based adjuvants. The complex immune environment of the gut-associated lymphoid tissue has the potential to induce broad and diverse immune responses. Therefore, we aimed to explore the potential of zinc sulfate as an oral adjuvant to enhance intestinal mucosal immunity and complement the effects of intramuscular (IM) FMD vaccination. Methods: We conducted serological analyses on mice and pigs, measuring secretory IgA (sIgA) levels and evaluating the expression of mucosal immunity-related genes in pigs. These assessments were used to investigate the systemic and mucosal immune responses induced by oral zinc sulfate administration in combination with an IM FMD vaccine. Results: This combination strategy significantly increased structural protein antibody titers and virus neutralization titers in experimental animals (mice) and target animals (pigs) across early, mid-, and long-term periods. Additionally, this approach enhanced the expression of key cytokines associated with mucosal immunity and increased sIgA levels, which are critical markers of mucosal immunity. Conclusions: Oral zinc sulfate administration may synergize with inactivated FMD vaccines, leading to sustained and enhanced long-term immune responses. This novel strategy could reduce the frequency of required vaccinations or allow for a lower antigen dose in vaccines, effectively stimulating the mucosal immune system and boosting systemic immunity. This approach has the potential to improve the overall efficacy of commercial FMD vaccines.

Beneficial effect of oral administration of zinc sulfate on 5-fluorouracil-induced gastrointestinal mucositis in rats.

This experimental study explored the potential of oral zinc sulfate to protect the gut mucosa from 5-fluorouracil (5-FU)-induced degenerative lesions in Wistar rats. Female Wistar rats were used and divided into 2 interventional groups (Z with 6 animals and F with 5 animals) and one control group (M with 5 rats). After 2 hours of fasting, group Z received via oral gavage 1.5 ml of solution, corresponding to 15 mg zinc sulfate for 9 consecutive days. Groups F and M received only the vehicles. On day 3, 400 mg/kg of 5-FU was administered intraperitoneally to groups Z and F. Tissue samples were collected from the duodenum, jejunum, colon and liver. Histological assessment for each gastrointestinal tract segment was determined semi-quantitatively by rating 11 histological features from normal (0) to severe (3). The independent groups were analyzed using the Kruskal-Wallis test and the Mann-Whitney U-test, with a Bonferroni correction for alpha (p ≤ 0.016). In group F the jejunum was the most affected area with a mean histological score of 27 (25-32). In the Z group, significantly lower histological scores were obtained compared with group F (duodenum Z vs. F: U = 0, p = 0.004; jejunum Z vs. F: U = 0, p = 0.006 and colon: Z vs. F: U = 0, p = 0.005). Graded liver necro-inflammatory lesions were significantly lower in group Z compared with group F (U = 0, p = 0.004), suggesting fewer bacterial intestinal translocation processes. Zinc sulfate has a beneficial role, decreasing the severity of gut mucosal injuries induced by 5-FU in Wistar rats.

Effects of Two Different Doses of Zinc Sulfate on Serum Troponin I 3 Enzyme Level and Cardiac Malondialdehyde Contents in Mitoxantrone-Induced Cardiotoxicity in Rats

Abstract
 Mitoxantrone is an antitumor agent used in the treatment of breast and prostate cancer, acute leukemia, lymphoma, and also in the treatment of multiple sclerosis due to its immunosuppressive properties. The mitoxantrone's cardiotoxicity is irreversible, dose-dependent, and it may occur years after treatment. Zinc is considered as an essential mineral for cell division and the synthesis of DNA and protein; furthermore, such mineral has an important role in states of cardiovascular diseases; and may have protective effects in coronary artery disease and cardiomyopathy.
 Objective: The current study is designed to investigate effects of two different doses of zinc sulfate on mitoxantrone-induced cardiotoxicity in rats.
 Methods: Forty-eight (48) adult rats of both sexes were utilized in this study; the animals were randomly divided into six groups of 8 animals each. Group I: distilled water (negative control). Group II: orally-administered zinc sulfate (15mg/kg/day) Group III: orally-administered zinc sulfate (30mg/kg/day) Group IV: Intraperitoneally injected with a mitoxantrone at a dose (2.5 mg/kg) to reach total cumulative dose of 7.5 mg/kg on day 20. Group V: Orally-administered zinc sulfate at a dose (15mg/kg/day) and an intraperitoneal injection of mitoxantrone at a dose (2.5 mg/kg) was administered to reach total cumulative dose of 7.5 mg/kg on day 20. Group VI: Orally-administered zinc sulfate at a dose (30 mg/kg/day), and an intraperitoneal injection of mitoxantrone at a dose (2.5 mg/kg) to reach total cumulative dose of 7.5 mg/kg on day 20.
 Forty-eight (48) hr after the end of treatment duration (i.e. at day 22 nd), each animal was euthanized by diethyl ether and ketamine. Then, after cervical dislocation, blood was obtained by intracardiac puncture and then serum was prepared to estimate cardiac troponin I 3 enzyme activity levels; and the heart of each animal was excised for homogenate preparation to estimate of malondialdehyde contents.
 Results: Oral administration of zinc sulfate [(15mg/kg/day with total cumulative dose (7.5 mg/kg) of mitoxantrone] (Group V) resulted in a non-significant (P>0.05) difference in serum activity level of troponin I 3 enzyme and malondialdehyde contents in cardiac tissue homogenate compared to the corresponding serum enzyme activity level and contents in group of rats intraperitoneally injected with total cumulative dose of 7.5 mg/kg of mitoxantrone (Group IV). In contrast, there were significant reduction (P<0.05) in serum activity level of troponin I 3 enzyme and malondialdehyde contents in cardiac tissue homogenate of rats orally-administered zinc sulfate [(30 mg/kg/day) with total cumulative dose (7.5mg/kg) of mitoxantrone] (Group VI) compared to the corresponding enzyme activity levels and contents in group of rats intraperitoneally-injected with total cumulative dose of 7.5mg/kg of mitoxantrone (Group IV).
 Conclusion: zinc sulfate at a dose (30 mg/kg/day) diminishes the cardiotoxicity induced by mitoxantrone via a free radical scavenger property but it is non signifant compared to (15 mg/kg/day) .

A case of acquired acrodermatitis enteropathica with a normal serum zinc level but a low level in the hair

Acrodermatitis enteropathica (AE) is a rare autosomal recessive disorder of early infancy, and is characterized by periorificial dermatitis, alopecia, and intractable diarrhea. Serum zinc levels are usually low in untreated patients and the oral administration of zinc sulfate can clear skin lesions and other symptoms. Although premature and cow's milk-fed infants are at particular risk of developing AE, there have been a few reports about AE in term and breast-fed infants. We report a case of transient AE in a 4-month-old breast-fed infant. This patient suffered from diarrhea and dermatitis for more than a month. Her skin lesions were erythematous, scaly, crusted, psoriasiform, eczematous, with an eruption at the chin, and a periorificial disposition with involvement of the flexural areas of lower extremities. Her serum zinc level was almost normal at 129μg/dL (reference range: 60-121μg/dL), but the zinc level in her hair was low: 8 mg percent (reference range: 10-21 mg percent). Skin biopsy findings were consistent with AE. Seven days after zinc supplementation, the skin lesions and diarrhea improved. The authors recommend that a clinical trial of zinc supplementation be considered in cases where there are suspicious of AE, even when the serum zinc level is normal.

Alteration in serum and bone component findings induced in streptozotocin-diabetic rats is restored by zinc acexamate

The effect of zinc acexamate in streptozotocin (STZ)-induced diabetic rats was investigated. Rats received a single subcutaneous administration of STZ (6.0 mg/100 g body weight), and the animals were orally administered once daily for 14 days with zinc acexamate (2.5, 5 or 10 mg/100 g body weight). The administration of STZ caused a significant increase in serum glucose, triglyceride and calcium levels and a significant decrease in body weight, serum zinc and inorganic phosphorus levels, indicating diabetic condition. Moreover, calcium content, alkaline phosphatase activity and deoxyribonucleic acid (DNA) content in the femoral-diaphyseal and -metaphyseal tissues were significantly reduced in STZ-diabetic rats. The change in these serum and bone components of STZ-diabetic rats was significantly restored by the oral administration of zinc acexamate (2.5, 5 or 10 mg Zn/100 g body weight). The restoration of bone components was not seen by the oral administration of zinc sulfate (2.5 mg Zn/100 g) for 14 days. Moreover, when the femoral-diaphyseal and -metaphyseal tissues obtained at 14 days after STZ administration were cultured for 48 h in a medium containing either vehicle or zinc acexamate (10(-5) M), the femoral calcium content and alkaline phosphatase activity were significantly increased in vitro. The effect of zinc acexamate was completely abolished in the presence of cycloheximide (10(-6) M), an inhibitor of protein synthesis. The present study demonstrates that the oral administration of zinc acexamate has a preventive effect on STZ-induced diabetic condition in rats, and that it can restorate bone loss of STZ-induced diabetes in vivo.

Zinc amplifies mSOD1-mediated toxicity in a transgenic mouse model of amyotrophic lateral sclerosis

Transgenic mice overexpressing the human mutated form (G93A) of Cu,Zn-superoxide dismutase (mSOD1) develop motor neuron degeneration resembling amyotrophic lateral sclerosis. In vitro studies have shown that mSOD1-induced, reactive oxygen species-mediated apoptosis of motor neurons depends on the presence of copper and the relative absence of zinc. Oral intake of zinc sulphate induces the expression of metallothioneins, enzymes that decrease oxidative stress, and leads to higher serum zinc, and lower copper levels. We therefore tested the effect of chronic oral administration of zinc sulfate (0.075 and 0.375 g/kg) on disease onset and survival of mSOD1 transgenic mice. We observed that zinc sulfate, rather than prolonging survival, decreased survival. We conclude that zinc sulfate amplifies the mSOD1 transgenic mouse phenotype. This finding may shed more light on the role of zinc in mSOD1-mediated toxicity.

Alternation in bone components with increasing age of newborn rats: role of zinc in bone growth

The effect of zinc on bone growth in newborn rats supplied with lactation by maternal rats was investigated. Newborn rats were killed between 1 and 35 days after birth. Increasing age caused a significant increase in zinc content, calcium content, and alkaline phosphatase activity in the femoral-diaphyseal and metaphyseal tissues, while the bone deoxyribonucleic acid (DNA) content was significantly decreased because of elevation of mineral content. Oral administration of zinc sulfate (2.0mg/100g body weight; four times at 24-h intervals) to maternal rats from 1 day after birth induced a significant increase in zinc, alkaline phosphatase activity, DNA, and calcium content in the femoral-diaphyseal and metaphyseal tissues of newborn rats compared with those 7 or 14 days old. The results indicate that the increase in bone components results from lactation with zinc-containing milk of maternal rats. The femoral-metaphyseal tissues of newborn rats obtained at 7 days after birth were cultured for 24h in a medium containing either vehicle or zinc sulfate (10(-6) to 10(-4) M) in vitro. Bone alkaline phosphatase activity and calcium and DNA content were significantly increased by zinc addition. These increases were completely prevented by the presence of dipicolinate (10(-3) M), a chelator of zinc ion, or cycloheximide (10(-6) M), an inhibitor of protein synthesis. The present study suggests that zinc plays a role in the development of bone growth in newborn rats.

Effect of Zinc on Experimental Acute Pancreatitis in Rats.

The effects of zinc on acute pancreatitis were investigated in rats with cerulein-induced pancreatitis and taurocholate+trypsin-induced pancreatitis. The endogenous zinc concentrations in the serum and pancreas after the onset of acute pancreatitis was not different from those in normal rats. Orally administered zinc sulfate was well absorbed and was taken up by the pancreas in normal rats as well as in rats suffering from acute pancreatitis. Oral administration of zinc sulfate before induction of acute pancreatitis reduced the serum amylase activity and the wet weight of the pancreas in rats treated with cerulein or taurocholate+trypsin. Oral administration of zinc sulfate after the induction of acute pancreatitis also reduced the pancreatic wet weight in rats with cerulein-induced pancreatitis, and decreased the mortality rate in rats with taurocholate+trypsin-induced pancreatitis. N-(3-aminopropionyl)-L-histidinato zinc (polaprezinc), a chelate of zinc and L-carnosine, also decreased the serum amylase activity and pancreatic wet weight in both types of pancreatitis. These data suggest that zinc compounds may have a therapeutic effect on acute pancreatitis.

Zinc Enhancement of Genistein’s Anabolic Effect on Bone Components in Elderly Female Rats

1. The effect of genistein on the bone components in the femoral-metaphyseal and diaphyseal tissues of elderly female rats was investigated. 2. The oral administration of genistein (100 and 200 μg/kg body weight) for 3 days to rats caused a significant increase in alkaline phosphatase activity, deoxyribonucleic acid (DNA) and calcium contents in the femoral-metaphyseal and diaphyseal tissues. A dose of 50 μg genistein/kg appreciably increased alkaline phosphatase activity and DNA content in the metaphyseal but not the diaphyseal tissues. 3. Alkaline phosphatase activity, DNA and calcium contents in the femoral-metaphyseal and diaphyseal tissues were significantly elevated by the oral administration of zinc sulfate (5.5 mg Zn/kg) for 3 days. The effect of zinc on increasing bone DNA and calcium contents was synergistically enhanced by the simultaneous administration of genistein (100 μg/kg). 4. The stimulatory effect of zinc sulfate (10 −5 M) or genistein (10 −5 M) on bone calcium content was also seen in a culture system using the femoral-metaphyseal and diaphyseal tissues in vitro. This effect was completely prevented by the presence of cycloheximide (10 −6 M). 5. The present findings suggest that genistein has an anabolic effect on bone components and that the effect is enhanced by zinc, owing to its stimulating effect on bone protein synthesis.

Zinc decrease and bone metabolism in the femoral-metaphyseal tissues of rats with skeletal unloading.

Whether the decrease of zinc content in the femoral-metaphyseal tissues of rats with skeletal unloading is involved in the alteration of bone metabolism was investigated. Skeletal unloading was designed using the model of hindlimb suspension in rats. Animals were fed for 4 days with the unloading. The metaphyseal zinc content were significantly decreased by the unloading. Zinc accumulation in the metaphyseal tissues by a single oral administration of zinc sulfate (20 mg Zn/100 g body weight) was partially depressed by the unloading, although serum zinc concentration was higher than that in normal rats, suggesting an impaired movement of zinc from serum into bone tissues by the unloading. Skeletal unloading caused a significant decrease of alkaline phosphatase activity and deoxyribonucleic acid (DNA) content in the metaphyseal tissues. These decreases were completely restored by addition of zinc sulfate (10(-4) M) or beta-alanyl-L-histidinato zinc (AHZ; 10(-5) M) in a culture medium with the metaphyseal tissues in vitro. The effects of zinc compounds were abolished by the presence of cycloheximide (10(-8) M), suggesting that the zinc effect is based on a newly synthesized protein. Dipicolinate (10(-4) and 10(-5) M), a potent zinc-chelating agent, caused an appreciable decrease of zinc content and alkaline phosphatase activity in the metaphyseal tissues. This decrease was restored by zinc supplement. The present results suggest that the skeletal unloading-induced decrease of zinc content in the femoral-metaphyseal tissues plays a role in the deterioration of bone metabolism in the unloaded rats.

Immunodeficiency and plasma zinc levels in children with Down's syndrome: A long-term follow-up of oral zinc supplementation

To evaluate the possible effect of zinc treatment on immune disorders in children with Down's syndrome (DS), 38 noninstitutionalized DS children were investigated. Twentyfour patients (63.2%) had plasmatic zinc levels lower than 0.70 μg/dl (“hypozinkemic,” LZn) and 14 patients (36.8%) had levels higher than 0.75 μg/dl (“normozinkemic,” NZn). No correlation was found between the zinc deficiency and recurrence and/or intensity of infections. The absolute numbers of peripheral lymphocytes, the percentages of B lymphocytes, total T cells, and serum IgG, IgA, and IgM levels did not differ between the DS children and the controls. Eight (21%) patients had CD4+ T cell counts below the lowest value for the controls. Seventeen (44%) DS patients had increased levels of CD8+ T cells. The mean percentage of Leu 7+ cells in DS subjects (22.8 ± 12.9%) was significantly higher than that in controls (15.8 ± 4.8%) ( P < 0.01). Notably, Ig levels and numbers of lymphocytes in each subset did not show any significant difference in NZn and LZn trisomic subjects. On the contrary the peripheral blood mononuclear cells (PBMCs) from LZn DS children showed a significantly lower proliferative response to phytohemagglutinin (PHA) (S.I. = 23.4 ± 22.4) than that of PBMCs from NZn DS children (S.I. = 46.1 ± 21.5, P < 0.01). A significant increase in DNA synthesis was obtained after oral administration of zinc sulfate (20 mg/kg/day, for 2 months). The lymphocyte response to PHA appeared to be normal in all patients up to 6 months after the end of the zinc treatment and it became low in half of the patients 22 months after therapy.

Aging affects cellular zinc and protein synthesis in the femoral diaphysis of rats

To clarify the effect of aging on bone metabolism, alteration of the cellular zinc content and protein synthesis was examined in the femoral diaphysis of 3- and 30-week-old male rats. The cellular zinc content in bone tissue markedly decreased in 30-week-old compared to 3-week-old rats. When the bone tissue from older rats were cultured with [3H]leucine, incorporation of [3H]leucine into the acid-insoluble residues was less than for weanling rats. This decrease was partly restored by the oral administration of zinc sulfate (0.5, 1.0, and 2.0 mg Zn/100 g body weight) to elderly rats for 3 days. An increase of in vitro [3H]leucine incorporation by bone tissues obtained from the rats that had received zinc (2.0 mg/100 g) was blocked by cycloheximide (10(-6) M) or dipicolinate (10(-3) M), a chelator of zinc. These results suggest that bone protein synthesis declines with age, and that this decline may be based partly on the decrease in bone cellular zinc.

The role of zinc as a stimulating factor in bone formation.

The role of zinc as a stimulatory factor on bone formation was reviewed. Bone growth retardation is a common finding in various conditions associated with zinc deficiency. The mechanism of zinc action on bone metabolism, however, has not been clarified so far. The oral administration of zinc sulfate (0.5-10 mg Zn/100 g body weight) to weanling rats can produce an increase in dry weight, alkaline phosphatase activity, calcium, collagen and deoxyribonucleic acid (DNA) contents in the femoral diaphysis, indicating that zinc has a stimulatory effect on bone formation and calcification. In tissue culture by using the calvaria from weanling rats, it has been demonstrated that zinc (10-6-10-4M) can stimulate bone protein synthesis, and that the zinc effect is based on activation of aminoacyl-transfer ribonucleic acid (tRNA) synthetase. The depletion of endogenous zinc in bone cells by treatment with dipicolinate, a chelator of zinc, can retard the synthesis of bone protein. Zinc is an essential factor in the systhesis of bone protein. Increasing age induces the deterioration of bone metabolism, and it decreases bone cellular zinc and protein systhesis. These decreases, however, can be restored by supplement of zinc. Thus, it has been introduced that zinc, an essential trace element, plays an important role in the stimulation of bone formation.

Effect of Topical Application of Glycine and Proline on Recalcitrant Leg Ulcers of Prolidase Deficiency

<h3>To the Editor.—</h3> The most important dermatologic problem of prolidase deficiency¹is chronic recurrent leg ulcers that are recalcitrant in healing. We used 5% glycine-5% proline ointment on leg ulcers with excellent results. <h3>Report of a Case.—</h3> The patient, now a 22-year-old woman, is the same patient as described previously.¹She had never been free of recalcitrant leg ulcers despite various conventional therapies including topical application of antibiotics (gentamicin sulfate, colistin sulfate, polymyxin B sulfate, etc), leg bath in 0.01% potassium permanganate solution, oral administration of zinc sulfate (180 mg daily), and/or ascorbic acid (3 g daily). Oral L-proline (1 g daily) was also tried for two months with no apparent benefit. We decided to use topical proline and then a combination of topical proline and glycine on her leg ulcers. L-proline and/or L-glycine ground with a mortar and pestle was mixed in liquid paraffin (30 g) and

Zinc absorption after oral administration of zinc sulfate.

The administration of 200 mg of ZnSO4.7H2O to six normal healthy males gave rise to increased serum zinc levels when this drug was taken in a fasting state, whereas administration during a light meal caused no increased levels.

Zinc accumulation and succinate dehydrogenase activation in hepatic mitochondria of rats orally administered zinc sulfate.

The changes of enzyme activities in subcellular fractions of rat liver were investigated after a single oral administration of zinc sulfate (20 mg Zn/100 g body weight). Zinc contents in the fractions of plasma membrane, nuclei, mitochondria, microsomes and cytosol were significantly increased 3 h after zinc administration. On the other hand, a significant decrease of the microsomal glucose-6-phosphatase activity and a remarkable elevation of the mitochondrial succinate dehydrogenase activity were caused by zinc administration, while the activities of the plasma membrane Ca2+-adenosine triphosphatase (ATPase), nuclear ribonucleic acid (RNA) polymerase and cytosolic acid phosphatase were not significantly altered. At the lowest dose (5 mg Zn/100 g) used in this experiment, the microsomal glucose-6-phosphatase activity was not significantly decreased, while the mitochondrial succinate dehydrogenase activity was markedly increased. Also, activation of succinate dehydrogenase in the liver mitochondria was observed at 12 h after zinc administration (10 mg Zn/100 g). The present study indicates that zinc taken up by the liver cells accumulates in the mitochondria and the metal may have an effect on the mitochondrial functions.

Hypocalcemic effect of zinc and mechanism in rats.

The effect of zinc on serum calcium was investigated after a single oral administration of zinc sulfate in rats. Zinc (5, 10, and 20 mg Zn/100 g body weight) administration produced a significant decrease of serum calcium. This effect of zinc was not inhibited by thyroparathyroidectomy. Zinc administration resulted in a significant increase in calcium content of lungs and muscle but it was not significant in liver, kidneys, spleen and heart. Intestinal calcium absorption and bile calcium excretion was not affected by zinc administration. However, the urinary calcium excretion after zinc administration decreased markedly. On the other hand, zinc administration caused a remarkable elevation of calcium content in gastric secretion. This effect was dose-dependent (5 and 10 mg Zn/100 g). However, an increase in gastric calcium after zinc administration was completely prevented by atropine (0.1 micrograms/100 g) treatment, which also showed a marked inhibition of hypocalcemic effect of zinc. Meanwhile, acetylcholine (4.0 micrograms/100 g) administration caused a significant decrease of serum calcium by zinc administration is mainly based on an increase in gastric calcium secretion.

Zinc metabolism in the liver of rats orally administered zinc sulfate.

Zinc metabolism in rat liver was investigated after a single oral administration of zinc sulfate. After the administration of 20 mg Zn per 100 g body weight, the zinc accumulated in the liver and pancreas, but not significantly in the kidneys, heart, spleen or lungs. The amount of zinc excreted into the bile was much less than that accumulated in the liver. On the other hand, the elevation of zinc content in the serum caused a significant increase of zinc in the plasma membrane and the cytosol fractions of the liver cells. However, additional increase of zinc in the serum did not further enhance the elevation of zinc content in the plasma membrane and the cytosol fractions. Upon gel filtration on Sephadex G-75 of the serum and cytosol obtained after zinc administration, the accumulated zinc in the serum was mainly eluted at the void volume, while the metal in the cytosol was largely eluted at 1.8 times the void volume, suggesting that the protein-bound zinc in the serum is not directly transported into the liver cells. The present study suggests that the liver is a target organ of zinc in rats and that zinc taken up by the liver cells is stored by binding of the metal to cytosolic proteins.

Lead, Zinc, and Erythrocyte δ-Aminolevulinic Acid Dehydratase: Relationships in Lead Toxicity

A lead-intoxicated patient with extremely high blood lead levels and unexpectedly mild symptoms was studied prior to and following treatment with calcium disodium edetate (ethylenediaminetetraacetic acid) and then prior to and following oral administration of zinc sulfate. During chelation therapy, erythrocyte (delta)-aminolevulinic acid dehydratase (ALAD) activity decreased as blood lead levels fell. Urinary excretion of zinc increased and was more than 3.5 times greater than that of lead. The ratio of blood lead to serum zinc was greatest (1.47) when ALAD activity was lowest. Oral administration of zinc sulfate following chelation therapy resulted in a significant increase in mean ALAD activity. In vitro additions of zinc chloride to the patient's erythrocytes resulted in reactivation of ALAD activity. These studies suggest that zinc is an important element in the ALAD system in man. Zinc may play a protective role in lead toxicity, and zinc supplementation may be a useful adjunct to chelation therapy for lead toxicity.

Effect of Zinc Sulfate on Tensile Strength of Incised Wounds: An Experimental Study

SummaryTo evaluate the effect of oral administration of zinc sulfate on tensile strength of incised wounds experiments were conducted on 50 albino rats. The results have been discussed and the difference between the methodology of the przsent work and the reported literature pointed out.