Boron and calcium chloride as possible ameliorators of fluoride toxicity in Wistar rats

  • Indian Council of Agricultural Research National institute of Veterinary Epidemiology and Disease Informatics, Bengaluru, India
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Fluorosis is an endemic health problem for both humans and livestock in some parts of the world including India. This fast expanding problem needs remedial measures. Though limited reports suggest ameliorative effect of boron (B) and calcium (Ca) against fluoride (F) toxicity in animals, still there is a need for long duration study to understand the possible mechanism of action. Here, we did the same; studied the ameliorative effect of B and Ca on F toxicity in Wistar strain (Rattus norvegicus) rats. Forty-eight male Wistar albino rats were divided randomly into six groups. The group T1 was given normal water (control) while the groups T2-T6 were supplemented with F through water @ 30 ppm (as sodium fluoride), 30 ppm F+ 50 ppm B (as sodium borate), 50 ppm B, 30 ppm F+ 50 ppm calcium chloride and 50 ppm calcium chloride, respectively. After four months, all the rats were sacrificed and blood, teeth, femur bone and liver were collected and analyzed for mineral content. Fluoride toxicity significantly (P <0.05) reduced phosphorus content in bone, calcium content in liver, and superoxide dismutase (SOD) activity in plasma. However, F toxicity significantly (P <0.05) increased phosphorus and glucose content in plasma, and calcium and magnesium content in teeth and fluoride content in liver. Boron and calcium chloride as ameliorating agents significantly (P <0.05) reduced the fluoride content in all the internal organs and also significantly reduced the elevated level of glucose and phosphorus in plasma and improved SOD activity in plasma. It is concluded that toxic effect of F is partially ameliorated by supplementation of 50 ppm of B or CaCl2.

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The aim of the present study was to assess the effect of fluoride toxicity on immunity and pathology of tissues in Wistar rats. Forty eight male Wistar albino rats aged 8 to 12 weeks were divided into four groups of twelve rats each. The group A, B, C and D were given normal water, 10 ppm, 30 ppm and 60 ppm of fluoride (Sodium fluoride), respectively daily in drinking water. At three, six and nine months of inducing fluoride toxicity, rats were injected with sheep red blood cells. Blood was collected after 14 days of injecting sheep red blood cells to assess humoral immunity. At nine months heparinised blood was used to assess cell mediated immunity. At three, six and nine months, rats were sacrificed and tissues collected for pathological study. Group D showed significant (P<0.05) decrease in haemagglutination titre at three months and no significant difference at six and nine months when compared to other groups. Significant (P<0.05) decrease in cell mediated immunity in rats of group D was observed. Effect of fluoride toxicity were observed in liver with vacuolar degeneration and hepatocellular necrosis, in kidney with casts in tubules and in spleen depletion of lymphocytes, in thyroid loss of colloid with degeneration of secretory epithelial cells and in thymus loss of lymphocytes and plasma cells. Histopathological changes in thymus and spleen concurred with immunological changes. Conclusively, fluoride toxicity induced by 60 ppm had effect on humoral and cell mediated immunity, and pathological changes in liver, kidney, spleen, thyroid and thymus in Wistar albino rat.
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It has been reported that boron may be beneficial for optimal calcium metabolism and, thus, optimal bone metabolism. Therefore, we designed a study to determine the effects of boron supplementation on blood and urinary minerals in athletic subjects and sedentary control subjects consuming self-selected typical Western diets. Serum phosphorus concentrations were lower in boron-supplemented subjects than in placebo-supplemented subjects. Compared with all other subjects, serum magnesium concentrations were greatest in the sedentary control subjects supplemented with boron and increased with time in all subjects. Exercise training diminished changes in serum phosphorus concentrations caused by boron supplementation. Calcium excretion increased over time in all groups combined, and boron excretion increased over time in all boron-supplemented subjects. The findings suggest that boron supplementation modestly affected mineral status, and exercise modified the effects of boron supplementation on serum minerals.
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An experiment was conducted to evaluate the effects of dietary boron (B) on growth performance, bone mechanical properties, and calcium (Ca) and phosphorus (P) metabolism in pigs. Thirty-six barrows were weaned at approximately 21 d of age and randomly assigned to receive one of three dietary treatments. Treatments consisted of 1) low-B basal diet (control), 2) basal + 5 mg B/kg diet, and 3) basal + 15 mg B/kg diet. Boron was supplemented as sodium borate. Barrows remained on their respective experimental diets throughout the nursery (35 d) and growing (30 d) phases of production. Blood samples were obtained from each barrow at the end of each phase. Following the 30-d growing period, eight barrows per treatment were transferred to stainless steel metabolism crates. Barrows had an adjustment period of 7 d, followed by a 7-d total collection of urine and feces. All barrows were fed at 90% of the previous ad libitum grower intake of the control animals during the adjustment and collection periods. At the end of the 7-d collection period, barrows were killed and femurs and fibulas were harvested for the assessment of bone mechanical properties. During the nursery phase, ADG and ADFI were increased (P < 0.05) by B supplementation. Boron did not affect (P = 0.34) feed efficiency during the nursery phase. During the growing phase, ADG and ADFI were increased (P < 0.05) by B supplementation. Boron did not affect (P = 0.97) feed efficiency during the growing phase. Boron did not affect (P = 0.44) bone ash percentage, but B supplementation increased (P < 0.05) bone ash P. Ultimate shear force of the fibula was increased (P < 0.05) in barrows supplemented with 15 mg B/kg diet compared to barrows fed diets supplemented with 5 mg B/kg diet. Apparent absorption and retention of Ca and P were not affected (P > 0.05) by dietary B. These data indicate that B supplementation to pigs can increase growth and bone strength without greatly affecting Ca and P metabolism.
The antidote action of boron and aluminum sulphate in chronic fluorine intoxication was tested on 8 groups of domestic pigs over a period of 13 months. To the diet of pigs, given 7 mg NaF/kg/d 4 and 8 mg B/kg/d and 0.1 g of aluminum sulphate was added as an antidote. NaF feeding caused chronic bone fluorosis. Although boron did not lead to reduction in fluorine storage in the skeleton, it exerted a certain detoxicating effect due to formation of less toxic boron fluorine complexes. Respecting the skeletal system, direct F action (increase of bone mass) is, at least partially, compensated by direct boron action upon bone (decrease in bone mass with reduced parathyroid activity). Aluminum sulphate reduces F absorption and F retention in the skeleton by 25 to 29%; concurrent inhibition of calcium absorption from the intestine results in secondary hyperparathyroidism and decrease in bone mass. According to these experiments, boron or aluminum sulphate are unsuitable prophylactically in humans chronically exposed to fluoride because of individual reaction to fluoride and because of the toxic action of boron and aluminum sulphate upon bone. Short-term administration of boron for more rapid detoxication in fluorosis cases may be permissible during exposure to fluoride and after exposure to the pollutant has been discontinued.
Prevalence of fluorosis in goat along with degree of fluoride contamination of water and fodder near an aluminium smelter plant, was studied. The fluoride contamination of water sample within 10 km of area, was above the safe level of 1 ppm. Hence, the increased fluorosis in the area may have been due to increased fluoride in fodder and water levels.
Livestock sharing man's environment are exposed to an array of toxic pollutants which may be hazardous to their health and production. The health effects of pollution in livestock vary from subtle or chronic intoxication to overt acute toxicities depending on source and kind of pollutant, extent and route of exposure extent and degree of other interacting agents, and species, age, physiology and nutrition of the exposed livestock population. Residue of pollutants in livestock products adversely effect their quality and cause potential threat to public health due to contamination of food chain. In India, problem of pollution is related to poorly planned developmental projects and overuse of natural resources by ever-increasing human population. Review of the work done during the 5 decades of post-independence indicated emerging trend of human and livestock health problems due to pollution in the country. Acute and chronic lead toxicosis, fluorosis and pesticide poisoning have been recognised as major health hazards of pollution in livestock with the increasing frequencies in recent past indicating growing threat of pollution to the livestock health. Scientific data also revealed residual effects of pollutants such as toxic heavy metals and pesticides in animal food products. However, as compared to medical data, fewer studies have been conducted to evaluate ill effects of pollution in livestock in the country. There is a need for intensive studies and also to make recommendations as to how best to limit ill effects of pollution in livestock.
The fourth edition of this important book covers the advances in livestock mineral nutrition, updated with more illustrations and additional material on the relationship between livestock and man. Recent developments are discussed, such as increasing the 'mineral value' of feeds by the use of additives and enhancing mineral availability through the use of organic sources of trace elements. The concept of the 'mineral footprint' of livestock production is introduced and methods of mineral feeding that lower environmental pollution are presented. Opportunities and problems in manipulating the mineral content of livestock to improve the mineral status of consumers are also addressed. The book is an essential resource for researchers and students in animal nutrition, agriculture and veterinary medicine, and a useful reference for those concerned with human nutrition and environmental protection.
The present study was conducted on 42 postmenopausal women subjects in Vailapally village, Nalgonda district, Andhra Pradesh, India, an endemic fluorotic area (water fluoride >4 ppm) and 34 postmenopausal women of nonfluorotic villages (water fluoride <0.4 ppm) of the Nalgonda area. The age group of the recruited subjects was 48-58 years and their years since menopause (YSM) was <10 years. Serum levels of fluoride (F), total alkaline phosphatase (ALP), tartarate resistant acid phosphatase-5b (TRAP-5b), catalase (CAT), glutathione-S-transferase (GST) and malondialdehyde (MDA) were estimated for bone mineral antioxidant and lipid peroxidation status. Significantly increased bone turnover markers ALP, TRAP-5b (p<0.01), and oxidative stress were observed with decreased levels of CAT and GST (p<0.01) activity in postmenopausal women residing in the fluorotic village. Significantly elevated levels of MDA (p<0.01) in these women compared to those in the nonfluorotic village indicated an increase in lipid peroxidation under fluoride stress.
The fluoride ion (F), an environmental pollutant, affects the cytokine mRNA expression of macrophages in vitro, but it is not clear whether or not these effects occur in vivo. In this study, we examined the effects of F on cytokine mRNA expression in splenic macrophages of mice after subacute oral administration for 1 mo as well as determining serum F. BALB/c mice were administered F at 0, 1, 5, 25, and 125 ppm in their drinking water. At the end of the 1-mo administration, the serum F was determined. Each spleen was sampled, the lymphocytes were separated as non-adherent cells, and the macrophages were separated as adherent cells. The macrophages were activated by lipopolysaccharide and the lymphocytes were activated by phytohemagglutinin. After the activation and incubation, the RNA was extracted and cDNA was synthesized. We examined the mRNA expressions of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNFα) for macrophages and those of interferon-γ (IFN-γ) and IL-2 for lymphocytes by RT-PCR (reverse transcription polymerase chain reaction). The mean intake of food or water per body weight was significantly lower in the 125-ppm group compared to the other groups. The relative weights of spleens in the 1- and 5-ppm groups were significantly lower than those in the control. The mRNA expression of TNFα in the macrophages was lower in the 125- ppm group. There were no differences among the groups for the mRNA expression of IL-1β in macrophages and those of IFN-γ and IL-2 in lymphocytes. Significant lower relative weights of the spleens were observed in a non-dose-dependent manner. Although there was no statistically significant difference in the expression of mRNA of TNFα in macrophages among the groups, the value in the 125-ppm group was lower. Although F may affect TNFα expression in vivo, the inability to demonstrate this in the present study may have been due to the F concentration in the blood not being sufficiently high compared with the value which affected mRNA expression in macrophages in vitro.
The influence of sodium fluoride (NaF) on superoxide dismutase (SOD) in mitochondria from germinating mung bean seedlings was studied. Mitochondrial preparations were obtained from seedlings treated daily with 0 (control), 0.1, 0.2, 1, and 5 mM NaF for 72 hours. NaF at 0.1 mM caused a small but significant increase in SOD activity, whereas 1 and 5 mM NaF decreased the enzyme activity by 10 and 40%, respectively.
Simultaneous daily administration of 60 mg/kg fluoride and 23.1 mg/kg boron to rabbits in drinking water during a two month period does not materially alter the fluoride metabolism. In both fluoride and fluoride plus boron groups the fluoride digestive utilization coefficient (DUC), the fluoride levels in the urine, the fluoride retention and the fluoride content of bones increase. Only hyperfluoremia was less pronounced in the F+B group than in the animals receiving fluoride without boron. On the other hand, fluoride-induced changes in the calcium phosphorus metabolism were largely prevented in the F+B group: Hypocalcemia returned to near normal levels; calcium and phosphorus retention and the DUC for calcium and phosphorus, which had decreased in the fluoride group, became normal. There was no change in the urinary calcium excretion and the phosphorus renal reabsorption coefficient (PRC). They were normal or slightly below normal when fluoride was given by itself. When one group of rabbits was given daily doses of 40 mg F/kg and the other the same dose of fluoride plus 15.4 mg B/kg for seven months, hyperfluoremia, hypocalcemia, the skeletal radiologic and clinical changes encountered in the F group were corrected in the F+B group.
Normal female rats of Wistar strain (Rattus norvegicus) weighing between 150–200 g were treated with fluoride (Fl) contaminated drinking water (FW, 5.8 ppm), vitamin C (6 mg) and vitamin C (6 mg) + D (6 mg once a week) + calcium (6 mg) for 30 days. Fl water treatment to rats produced reduction in weights of ovaries, uterus, vagina, kidneys, and adrenal glands, circulating levels of estrogen, number of litters, fertility rate, and altered tissue and serum biochemistry compared to control rats. However, cholesterol concentrations of ovaries and adrenals increased significantly. The above altered parameters were restored partially/completely after exogenous feeding with vitamin C and vitamins (C + D) and calcium. The data suggest that Fl-induced adverse effects on reproductive and other organs in female rats, whereas vitamin C, vitamin D and calcium treatment ameliorated Fl toxicity. Therefore, vitamins (C and D) and calcium play an important role in prophylactic treatment of fluorosis.
The recovery from fluoride toxicity of white mice by strontium (Sr) and boron (B) was investigated. With the 2 mg NaF/kg body weight B.W./d treatment for 6 months, the body weights and the fluoride levels in livers of white mice had no significant changes in comparison with the control. However, the fluoride contents in bones sharply increased (p <0.01) after 1.5 months treatment. No significant variation in alkaline phosphatase (ALP) activity in serum was observed after 1.5 and 3.0 months NaF treatment, whereas, with NaF administration for 4.5 and 6.0 months, the ALP activities increased markedly (p <0.01). The ALP activity in kidneys was significantly higher than the control (p <0.01) after the white mice had maintained on water containing NaF for 1.5 months. When 2mg NaF/kg B.W./d was administered with 0.8 mg B/kg B.W./d and 1 mg Sr/kg B.W./d concurrently, fluoride levels in bones and ALP activities in serum and kidney was reduced compared with individual treatment of fluoride, which suggested that Sr and B could antagonize fluoride toxicity. The extent of recovery was somewhat more pronounced by B treatment than by Sr administration.
: The occurrence of superoxide dismutase (SOD) in the earthworm Eisenia fetida has been demonstrated. The enzyme was inhibited when the worms were exposed to NaF in vivo and in vitro. Conversely, their exposure to NaF in vivo increased tissue glutathione (GSH) levels. Marked inhibition oc-curred when crude enzyme extract was treated with KCN, suggesting that the enzyme is a CuZnSOD.
: Treatment of male mice (Mus musculus) with sodium fluoride (NaF, 10 mg/kg body weight), alone or in combination with aluminium chloride (AlCl 3 , 200 mg/kg body weight), was investigated for its effects on gastrocne-mius muscle and liver. Recovery after one-month withdrawal of treatment and responses to some antidotes, viz calcium, ascorbic acid, and vitamin E ad-ministered alone or in combination were also studied. NaF alone or in combi-nation with AlCl 3 caused a significant decrease in protein levels and activity of succinate dehydrogenase (SDH) in liver and gastrocnemius muscle, thereby indicating altered protein and oxidative metabolisms in these tissues. Cholin-esterase activity declined significantly with all the treatments in both tissues, probably affecting the synaptic transmission due to altered acetylcholine re-lease or metabolism and altering muscle contraction. All three treatments caused changes in liver function as shown by a signifi-cant increase in serum transminases, accumulation of glycogen and inhibition of phosphorylase activity thereby indicating that carbohydrate metabolism was affected. Similar changes occurred in muscle tissue. Gastrocnemius muscle and liver were therefore affected by sodium fluoride, aluminium chlo-ride and in combination. Recovery was not significant on withdrawal of NaF + AlCl 3 treatment. How-ever, all three antidotes brought about significant recovery in the organs stud-ied. Individually, ascorbic acid was the most beneficial in bringing about pro-nounced recovery. Thus, intoxication induced by sodium fluoride and aluminium chloride is transient and reversible.
Chronic exposure to high fluoride (F(-)) may lead to local tissue disturbances, known as fluorosis. F(-) is an oxidising agent and a well-known reversible enzymatic inhibitor that interferes with the enzyme activity of at least 80 proteins. The goals of the current study were to evaluate whether F(-) exposure affected the oral glucose tolerance test (OGTT) in C57BL6 mice; and to determine the mechanisms at work in glucose homeostasis at the cellular level, in mouse pancreatic beta-cells (betaTC-6) exposed to F(-). Mice received 45 mgl(-1) F(-), as NaF, via drinking water, and cells were exposed for 12h to NaF (equivalent to 0, 0.007, 0.045, 0.180, 1.35 or 2.26 mM F(-)) at a basal or stimulatory glucose concentration (2.8 or 16.6mM, respectively). Mice showed marginal hyperglycemia an impaired glucose tolerance after 4 weeks of F(-) exposure, while beta-cells exposed to 1.35 and 2.26 mM F(-) had significantly lower insulin mRNA expression and subsequent secretion in the presence of the stimulatory glucose concentration. Western blot analyses did not show any alteration in the levels of glucose transporter-2 protein beta-cells on exposure to F(-)in vitro. However, oxidative stress evaluated by the functional activity of superoxide dismutase (SOD) and generation of the superoxide anion (O(2)(-)), showed significantly decreased SOD activity, in a dose-dependent manner. This was accompanied by an increase in the generation of O(2)(-), and decreased mitochondrial membrane potential in F(-) exposed cells. Insulin secretion was lower in beta-cells exposed to F(-), even in the presence of glibenclamide, the ATP-sensitive K(+) (K(ATP)) channel blocker, suggesting down-regulation of the K(ATP) channel in the cell. Exposure to high levels of F(-) in drinking water may decrease insulin mRNA and its secretion from beta-cells, and might therefore affect the OGTT.
Female rats were treated with fluoride for 100 days (between 21 and 121 days of age) replacing the water supply with a 5 mM NaF solution. Bone mass was assessed by destructive physical and chemical measurements on the whole skeleton, that gave an overall view not reported previously. Bone mass (dry, fat-free weight of the skeleton/100 g of body weight) increased 7% (P less than 0.001) with respect to control animals. This phenomenon was equally evident in the head, the axial and the appendicular skeleton. Fluoride treatment did not affect the ratio ashes/organic matrix. Treated animals showed a subtle disturbance of glucose tolerance as shown by glucose tolerance tests. The disturbance was manifest as high plasma and soft tissue levels of fluoride during the period of bone mass increase. Glucose tolerance was normalized when the maximum bone mass was achieved and plasma and soft tissue fluoride returned to control levels.
Recent findings are reviewed indicating that changes in dietary boron and magnesium affect calcium, and thus bone, metabolism in animals and humans. In animals, the need for boron was found to be enhanced when they needed to respond to a nutritional stress which adversely affected calcium metabolism, including magnesium deficiency. A combined deficiency of boron and magnesium caused detrimental changes in the bones of animals. However, boron deprivation did not seem to enhance the requirement for magnesium. In two human studies, boron deprivation caused changes in variables associated with calcium metabolism in a manner that could be construed as being detrimental to bone formation and maintenance; these changes apparently were enhanced by low dietary magnesium. Changes caused by boron deprivation included depressed plasma ionized calcium and calcitonin as well as elevated plasma total calcium and urinary excretion of calcium. In one human study, magnesium deprivation depressed plasma ionized calcium and cholesterol. Because boron and/or magnesium deprivation causes changes similar to those seen in women with postmenopausal osteoporosis, these elements are apparently needed for optimal calcium metabolism and are thus needed to prevent the excessive bone loss which often occurs in postmenopausal women and older men.
The influence of gastric acidity on the absorption of intragastrically administered fluoride was investigated in rats. Intact animals were pretreated with atropine or cimetidine to reduce gastric acid secretion or were given fluoride in NaHCO3 to reduce the acidity of the gastric contents. Compared with pentagastrin-treated animals or animals that received fluoride in 0.1 N HCl, their rate of fluoride absorption was markedly reduced as judged by lower plasma fluoride concentrations and areas under the time-plasma concentration curves, especially during the first hour after dosing. In crossover studies with the stomachs isolated in situ, fluoride absorption was at least 50% faster from a pH 2.1 buffer compared with its absorption from a pH 7.1 buffer. The findings are consistent with the hypothesis that fluoride is absorbed from the gastric lumen principally as the undissociated molecule, HF. The results may contribute to a more complete understanding of acute fluoride toxicity, the development of dental fluorosis and, perhaps, the use of fluoride in the treatment of osteoporosis.
In the insulin-secreting beta cell line RINm5F, sodium fluoride stimulated exocytosis in a concentration (5-15 mM)- and temperature-dependent manner. Depletion of aluminum with the chelator deferoxamine or addition of aluminum to the buffer failed to affect the NaF-stimulated insulin release. This suggests that stimulation of heterotrimeric G proteins or inhibition of phosphatases or other enzymes by fluoroaluminate, an analog of the phosphate moiety, is not involved in the insulinotropic action of NaF. Removal of extracellular Ca2+ suppressed the NaF-stimulated insulin release. However, nitrendipine, a blocker of L-type voltage-dependent Ca2+ channels, did not inhibit the NaF-stimulated insulin release and NaF did not cause any changes in the cytosolic free calcium concentration ([Ca2+]i). Decreasing [Ca2+]i with thapsigargin or increasing [Ca2+]i with ionomycin or a depolarizing concentration of KCl resulted in suppression or enhancement of NaF-stimulated insulin release, respectively. Furthermore, NaF enhanced Ca(2+)-induced insulin release in electrically permeabilized RINm5F cells. These findings indicate that the effect of NaF on exocytosis is dependent on [Ca2+]i, although NaF itself does not change [Ca2+]i. Inhibitors of protein kinase C, such as staurosporine and bisindolylmaleimide, in concentrations sufficient to block the effects of phorbol esters, did not attenuate the NaF-stimulated insulin release. Neither cellular cAMP content nor [3H]arachidonic acid release was increased by NaF. NaF-stimulated insulin release was synergistically enhanced by the activation of protein kinases A and C. Finally, trifluoperazine, an inhibitor of calmodulin and other Ca(2+)-binding proteins, inhibited the insulinotropic action of NaF in a concentration-dependent manner. Trifluoperazine (50 microM) and W-7 (100 microM) nullified the 10 mM NaF-stimulated insulin release. It is concluded that NaF evokes exocytosis by a novel mechanism of sensitization to Ca2+, possibly on a Ca(2+)-responsive protein that is sensitive to trifluoperazine and W-7, leading to exocytosis. Protein kinases A and C also act at this site or at a more distal point.
Thirty-two barrows (Duroc x Landrace x Yorkshire) were randomly divided into four groups, each of which included eight pigs. The groups received the same basal diet supplemented with 0, 100, 250 and 400mg/kg fluoride, respectively. The malondialdehyde (MDA) and glutathione (GSH) levels, antioxidant enzymes activities and zinc/copper superoxide dismutase (Cu/Zn SOD) mRNA content in the liver were determined to evaluate the fluoride hepatic intoxication. Results showed the increased lipid peroxides (LPO) level and the reduced GSH content, along with a concomitant decrease in the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px). Moreover, the level of hepatic Cu/Zn SOD mRNA was also significantly reduced. We suggest the mechanism of fluoride injuring the liver as follows: fluoride causes a decrease in Cu/Zn SOD mRNA and the reduced activities of antioxidant enzymes, leads to the declined ability of scavenging free radicals with excessive production of LPO, which seriously damages the hepatic structure and function.
The objective of this study was to consider the effects of boron (B) and calcium (Ca) supplementation on mechanical properties of bone tissues and mineral content of the selected bones in rats. Adult male Sprague Dawley rats underwent three different treatments with boron and calcium in their drinking water, while taking diet ad libitum for 4 weeks. Rats in the three treatment groups received 2 mg B/d, 300 mg Ca/d, and a combination of 2 mg B+ 300 mg Ca/d, respectively. After the experimental period body weights were recorded and bone mechanical properties were determined on the tibiae, femurs, and fifth lumbar vertebral bones and the mineral contents of these bones was calculated as the ash percentage. Better measurement of bone mechanical properties were observed for boron supplementation. The stiffness of the lumbar vertebral bones tended to increase in all groups and was significant for Ca supplementation. The significant maximal load obtained for boron in all bones indicates higher strength and less strength for apparently a high level of calcium, while this negative defect in the case of lumbar vertebral bones was corrected in the presence of boron. Highest mean energy to maximal load was shown with boron supplementation, demonstrating significant values with Ca group, and lower energy for the lumbar vertebral bones in Ca group in comparison with the controls. Less deformation at the yield points was shown in Ca group. There were no significant differences in ash weights among the four groups. Additional and longer studies are warranted to further determine the effects of supplemental boron with different calcium levels and possibly other minerals involved in bone mechanical properties in rats.
Bone healing after tooth extraction in rats is a suitable experimental model to study bone formation. Thus, we performed a study to determine the effects of boron (B) deficiency on bone healing by using this model. The first lower right molar of weanling Wistar rats was extracted under anesthesia. The animals were divided into two groups: +B (adequate; 3 mg B/kg diet), and -B (boron-deficient; 0.07 mg/kg diet). The animals in both groups were killed in groups of 10 at 7 and 14 days after surgery. The guidelines of the NIH for the care and use of laboratory animals were observed. The mandibles were resected, fixed, decalcified, and embedded in paraffin. Buccolingually oriented sections were obtained at the level of the mesial alveolus and used for histometric evaluations. Total alveolar volume (TAV) and trabecular bone volume per total volume (BV/TV) in the apical third of the alveolus were determined. Percentages of osteoblast surface (ObS), eroded surface (ES), and quiescent surface (QS) were determined. No statistical significant differences in food intake and body weight were observed. Histomorphometric evaluation found -B rats had 36% and 63% reductions in BV/TV at 7 and 14 days, respectively. When compared with +B rats, -B rats had significant reductions (57% and 87%) in ObS concomitantly with increases (120% and 126%) in QS at 7 and 14 days, respectively. The findings show that boron deficiency results in altered bone healing because of a marked reduction in osteogenesis.
An experiment was undertaken to evaluate the protective role of boron on the serum profile of buffalo calves fed a high fluoride ration. Twelve male Murrah buffalo (Bubalus bubalis) calves of 6-8 months age, divided into three groups of four calves in each, were fed basal diets and supplemented with sodium fluoride (NaF, 60 ppm) alone or in combination with borax (Na2B4O7.10H2O, 140 ppm) for 90 days. Boron (B) was added in the ration as borax to make @140 ppm boron (elemental B) on DM basis in treatment II. Dietary F caused a significant (p<0.05) depressing effect on serum Ca and Zn on day 90 which was improved with B supplementation. However, serum Fe and Cu did not show any significant change on F or F+B supplementation. The serum ALP and phosphorus level were increased significantly (p<0.05) on F feeding but declined significantly (p<0.05) when B was fed. The findings suggested beneficial effect of boron on serum minerals and ALP in buffalo calves fed high fluoride ration.
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