Influence of Zinc on the Biokinetics of 65Zn in Brain and Whole Body and Its Bio-distribution in Aluminium-Intoxicated Rats

The present study was designed to understand the influence of zinc (Zn) if any, on the biokinetics of ⁶⁵Zn in brain as well as whole body and its bio-distribution following aluminium (Al) treatment to rats. Male Sprague–Dawley rats weighing 140–160 g were divided into four different groups viz: normal control, aluminium treated (100 mg/kg b.wt./day via oral gavage), zinc treated (227 mg/L in drinking water) and combined aluminium and zinc treated. All the treatments were carried out for a total duration of 8 weeks. Al treatment showed a significant increase in fast component (Tb₁) but revealed a significant decrease in slow component (Tb₂) of biological half-life in brain as well as in whole body. However, Zn supplementation to Al-treated rats reversed the trend in both brain and whole body, which indicates a significant decrease in Tb₁ component while the Tb₂ component was significantly increased. Further, Al treatment showed an increased percent uptake value of ⁶⁵Zn in cerebrum, cerebellum, heart, liver and lungs whereas a decrease in uptake was found only in blood. On the other hand, there was a significant decline in ⁶⁵Zn activity in nuclear and mitochondrial fractions of brain of Al-treated rats. However, Zn treatment reversed the altered ⁶⁵Zn uptake values in different organs as well as in various subcellular fractions. The study demonstrates that Zn shall prove to be effective in regulating the biokinetics of ⁶⁵Zn in brain and whole body and its distribution at the tissue and subcellular levels in Al-treated rats.     

Effect of zinc on biological half-lives of 65Zn in whole body and liver and on distribution of 65Zn in different organs of rats following nickel toxicity

This study was designed to determine the effect of zinc on the biological half-lives of ⁶⁵Zn in whole body and liver and on distribution of ⁶⁵Zn in different organs of rats following nickel toxicity. Sprague-Dawley (SD) rats received either nickel in the form NiSO₄·6H₂O at a dose of 800 mg/L in drinking water, zinc in the form of ZnSO₄·7H₂O at a dose of 227 mg/L in drinking water, and nickel plus zinc or drinking water alone for a total duration of 8 wk. All of the rats were injected with a tracer dose of 0.37 MBq ⁶⁵Zn at the end of the treatment period. The effects of different treatments were studied on biological half-lives of ⁶⁵Zn in whole body and liver and on the distribution of ⁶⁵Zn in different organs of rats. In the present study, we have noted that nickel treatment to normal rats caused a significant decrease in the slow component (Tb₂) in liver, which improved following zinc supplementation. Nickel administration to normal-diet-fed animals caused significant lowering in the percentage uptake of ⁶⁵Zn values in the brain, liver, and intestine. However, the administration of zinc to nickel-treated rats improved the status of ⁶⁵Zn in different organs. The Tb₂ in the liver and the percentage uptake of ⁶⁵Zn values elevated following zinc supplementation to nickel-treated rats.     

Altered Uptake and Biological Half-Lives of 65Zn on Arsenic Exposure—Modulation by Zinc Treatment

The present study revealed the effects of zinc on the biokinetics of (65)Zn in rats following arsenic intoxication. The animals were segregated into four groups: group I--untreated controls, group II--arsenic treated (100 ppm as NaAsO(2) in drinking water), group III--zinc treated (227 mg ZnSO(4) per liter drinking water), and group IV--arsenic?+?zinc treated. Each rat was injected intraperitoneally with 1.85 MBq radioactivity of (65)Zn following 3 months of different treatments, and the radioactivity was determined using a suitably shielded scintillation counter. Arsenic treatment showed a significant increase in the fast component (Tb(1)) of the biological half-life of (65)Zn in liver, which remained unaltered in the whole body. Furthermore, arsenic treatment decreased significantly the slow component (Tb(2)) in the whole body, which remained unchanged in the liver. However, zinc supplementation to arsenic-treated rats normalized Tb(1) in the liver, but caused no change in Tb(2) in the whole body. Furthermore, the uptake values of (65)Zn were significantly increased in the liver, brain, kidney, and intestine following arsenic treatment, and the values in the liver and brain were decreased by zinc. Hence, zinc plays a significant role in regulating the biokinetics of (65)Zn in the liver and the whole body of arsenic-intoxicated rats.     

Assessing the Zinc solubilization ability of <Emphasis Type="Italic">Gluconacetobacter diazotrophicus</Emphasis> in maize rhizosphere using labelled <Superscript>65</Superscript>Zn compounds

Solubilization of insoluble zinc compounds like ZnCO₃ and ZnO by G. diazotrophicus was confirmed using radiotracers. The zinc compounds (ZnCO₃ and ZnO) were tagged with ⁶⁵Zn. ⁶⁵ZnCO₃ and ⁶⁵ZnO was effectively solubilized and the uptake of zn by the plants also more in G. diazotrophicus inoculated treatments compared to the uninoculated treatments. Three types of soils (Zn deficientsterile, Zn deficient-unsterile, and Zn sufficient-sterile) were used in experiment. Among the three soils, Zn deficient-unsterile soil registered maximum zinc solubilization compared to other two soils. This may be due to other soil microorganisms in unsterile soil. Application of ZnO with G. diazotrophicus showed better uptake of the nutrient.     

Effects of interaction between65Zn,cadmium, and copper in rats

Distribution and retention of zinc in the presence of cadmium and copper was studied in rats exposed repeatedly to these metals. The experiment was performed on white rats of the Wistar strain. The animals were divided into four groups/five rats each: 1)⁶⁵ZnCl₂; 2)⁶⁵ZnCl₂+CdCl₂; 3)⁶⁵ZnCl₂+CuCl₂; and 4) control group. Rats were administered sc every other day for two weeks:⁶⁵ZnCl₂−5 mg Zn/kg; CdCl₂−0,3 Cd/kg; and CuCl₂−2 mg Cu/kg. The zinc content was measured in rat tissues by γ-counting. Effect of Cd and Cu on subcellular distribution of zinc in the kidney and liver and on the level of metallothionein were also examined. Whole body retention of zinc under the influence of cadmium was lower than that observed in animals treated with zinc alone. However, copper increased twofold the whole body retention of zinc. Cadmium elevated the accumulation of zinc only in the kidneys nuclear fraction and liver soluble fraction. In the kidneys and liver, copper elevated the accumulation of zinc, in the nuclear, mitochondrial, and soluble fractions. The level of metallothionein-like proteins (MT) in the kidneys after a combined supply of zinc and copper was significantly increased with respect to the group of animals treated with zinc alone. These results indicated complex interactions between cadmium, copper, and zinc that can affect the metabolism of each of the metals.     

Intestinal transport of zinc in the diabetic rat

Zinc has been implicated to play a role in the pathogenesis and management of diabetes. Since the intestinal transport of several minerals as calcium, magnesium and strontium was found to be altered in the diabetic rats, we postulated that intestinal zinc transport may be also altered in the diabetic rat. Therefore, using $\text{in}$$\text{vivo}$ single pass perfusion technique we determined lumen to mucosa flux, net absorption and the mucosa to lumen flux of zinc in the small and large intestinal segments of diabetic rats, diabetic rats treated with insulin and in control rats. Tissue distribution of transported ⁶⁵Zn into various organs and tissue concentrations of native zinc in the groups of rats studied were determined. Our results indicate that lumen to mucosa flux (μmole/h/g wet weight) was decreased in all intestinal segments of the diabetic rats compared to controls. However, the total capacity (mμmole/h/cm length) was similar. The specific activity and total capacity of net absorption of zinc was similar in all intestinal segments of the rats studied. The reverse mucosa to lumen flux was significantly decreased in all segments of diabetic rats compared to corresponding values in control rats. Tissue distribution of ⁶⁵Zn following the perfusion study showed increased retention of ⁶⁵Zn in the liver, kidney and femurs of the diabetic rats compared to controls. Serum and tissue concentration of native zinc in various organs were similar in all groups of rats studied. The mechanism(s) responsible for these findings are discussed.     

Equivalent uptake of organic and inorganic zinc by monkey kidney fibroblasts, human intestinal epithelial cells, or perfused mouse intestine

Zinc (Zn) is recognized as an essential nutrient, and is added as a supplement to animal and human diets. There are claims that zinc methionine (ZnMet) forms a stable complex that is preferentially transported into tissues, and this has contributed to uncertainty about conflicting reports on the bioavailability of various Zn compounds. This study evaluated the cellular and intestinal uptake of inorganic and organic forms of Zn. Steady-state uptake of⁶⁵Zn by human intestine epithelial cells, and monkey kidney fibroblasts was not significantly different with zinc chloride (ZnCl₂), ZnMet, or zinc propionate (ZnProp) (P > 0.05). Uptake of⁶⁵Zn from zinc chelated with EDTA was significantly lower (P < 0.01). In live mice,⁶⁵Zn uptake by perfused intestine and deposition in intestine and liver showed no significant difference between ZnCl₂ and ZnMet. Equimolar [⁶⁵Zn]methionine and zinc[³⁵S]methionine were prepared according to a patented method that yields “ complexed” Zn. Cellular uptake of the radiolabeled methionine was <0.1% of the radiolabeled Zn from these complexes, indicating separate uptake of the Zn and methionine. Gel filtration did not distinguish between⁶⁵Zn in ZnCl₂, ZnProp, or reagent ZnMet, though feed-grade ZnMet containing >10% protein did give a higher-mol-wt form of⁶⁵Zn. Results of this study show equivalent uptake of Zn from inorganic and organic compounds, and support recent feed trials on Zn bioavailability.     

Biokinetics of <Superscript>90</Superscript>Sr after chronic ingestion in a juvenile and adult mouse model

The aim of our study was to define the biokinetics of ⁹⁰Sr after chronic contamination by ingestion using a juvenile and adult murine model. Animals ingested ⁹⁰Sr by drinking water containing 20 kBq l⁻¹ of ⁹⁰Sr. For the juvenile model, parents received ⁹⁰Sr before mating and their offspring were killed between birth and 20 weeks of ingestion. For the adult model, ⁹⁰Sr ingestion started at 9 weeks of age and they were killed after different ingestion periods up to 20 weeks. The body weight, food and water consumption of the animals were monitored on a weekly basis. Before killing and sampling of organs, animals were put in metabolic cages. ⁹⁰Sr in organs and excreta was determined by liquid scintillation β counting. Highest ⁹⁰Sr contents were found in bones and were generally higher in females than in males, and ⁹⁰Sr retention varied according to the skeletal sites. An accumulation of ⁹⁰Sr in the bones was observed over time for both models, with a plateau level at adult age for the juvenile model. The highest rate of ⁹⁰Sr accumulation in bones was observed in early life of offspring, i.e. before the age of 6 weeks. With the exception of the digestive tract, ⁹⁰Sr was below the detection limit in all other organs sampled. Overall, our results confirm that ⁹⁰Sr mainly accumulates in bones. Furthermore, our results indicate that there are gender- and age-dependent differences in the distribution of ⁹⁰Sr after low-dose chronic ingestion in the mouse model. These results provide the basis for future studies on possible non-cancerous effects during chronic, long-term exposure to ⁹⁰Sr through ingestion in a mouse model, especially on the immune and hematopoietic systems.     

<Superscript>65</Superscript>Zn<Superscript>2+</Superscript> transport by lobster hepato-pancreatic baso-lateral membrane vesicles

The lobster (Homarus americanus) hepato-pancreatic epithelial baso-lateral cell membrane possesses three transport proteins that transfer calcium between the cytoplasm and hemolymph: an ATP-dependent calcium ATPase, a sodium-calcium exchanger, and a verapamil-sensitive cation channel. We used standard centrifugation methods to prepare purified hepato-pancreatic baso-lateral membrane vesicles and a rapid filtration procedure to investigate whether ⁶⁵Zn²⁺ transfer across this epithelial cell border occurs by any of these previously described transporters for calcium. Baso-lateral membrane vesicles were osmotically reactive and exhibited a time course of uptake that was linear for 10–15 s and approached equilibrium by 120 s. In the absence of sodium, ⁶⁵Zn²⁺ influx was a hyperbolic function of external zinc concentration and followed the Michaelis-Menten equation for carrier transport. This carrier transport was stimulated by the addition of 150 M ATP (increase in K_m and J_max) and inhibited by the simultaneous presence of 150 mol l^–1 ATP+250 mol l^–1 vanadate (decrease in both K_m and J_max). In the absence of ATP, ⁶⁵Zn²⁺ influx was a sigmoidal function of preloaded vesicular sodium concentration (0, 5, 10, 20, 30, 45, and 75 mmol l^–1) and exhibited a Hill Coefficient of 4.03±1.14, consistent with the exchange of 3 Na⁺/1Zn²⁺. Using Dixon analysis, calcium was shown to be a competitive inhibitor of baso-lateral membrane vesicle ⁶⁵Zn²⁺ influx by both the ATP-dependent (K_i=205 nmol l^–1 Ca²⁺) and sodium-dependent (K_i=2.47 mol l^–1 Ca²⁺) transport processes. These results suggest that zinc transport across the lobster hepato-pancreatic baso-lateral membrane largely occurred by the ATP-dependent calcium ATPase and sodium-calcium exchanger carrier proteins.Communicated by: I.D. Hume     

Effects of increased pCO2 on zinc uptake and calcification in the tropical coral Stylophora pistillata

Zinc (Zn) is an essential element for corals. We investigated the effects of ocean acidification on zinc incorporation, photosynthesis, and gross calcification in the scleractinian coral Stylophora pistillata. Colonies were maintained at normal pH_T (8.1) and at two low-pH conditions (7.8 and 7.5) for 5 weeks. Corals were exposed to ⁶⁵Zn dissolved in seawater to assess uptake rates. After 5 weeks, corals raised at pH_T (8.1) exhibited higher ⁶⁵Zn activity in the coral tissue and skeleton, compared with corals raised at a lower pH. Photosynthesis, photosynthetic efficiency, and gross calcification, measured by ⁴⁵Ca incorporation, were however unchanged even at the lowest pH.     

Influence of Zn<Superscript>2+</Superscript>, Co<Superscript>2+</Superscript> and dimethylbenzimidazole on vitamin B<Subscript>12</Subscript> biosynthesis by <Emphasis Type="Italic">Pseudomonas denitrificans</Emphasis>

Previous research has confirmed that cobalt ion and dimethylbenzimidazole (DMBI) are the precursors of vitamin B₁₂ biosynthesis, and porphobilinogen synthase (PBG synthase) is a zinc-requiring enzyme. In this paper, the effects of Zn²⁺, Co²⁺ and DMBI on vitamin B₁₂ production by Pseudomonas denitrificans in shake flasks were studied. Present experimental results demonstrated that the addition of the above mentioned three components to the fermentation medium could significantly stimulate the biosynthesis of vitamin B₁₂. The concentrations of zinc sulphate, cobaltous chloride and DMBI in the fermentation medium were further optimized with rotatable orthogonal central composite design and statistical analysis by Data Processing System (DPS) software. As a result, vitamin B₁₂ production was increased from 69.36 ± 0.66 to 78.23 ± 0.92 μg/ml.     

A histidine supplement and regulation of the zinc status in Swiss random mice

The effects of histidine on the zinc status are controversial. In mice, we studied the effects of a moderate histidine supplement on the regulation of the zinc status using subcutaneously administered⁶⁵Zn. In animals fed a zinc-adequate diet, histidine supplement did not cause changes in the zinc status (zinc concentrations,⁶⁵Zn tissue distribution, and tissue specific activities). Neither effects on the regulation of the zinc status (⁶⁵Zn retention, excretion and biological half-life) could be demonstrated. However, the combination of a low zinc diet and moderate histidine supplementation caused changes in the regulation of the zinc status (lower⁶⁵Zn retention, associated with increased fecal excretion and a shorter biological half-life), aggravating the dietary deficiency (lower bone zinc, a shift in the⁶⁵Zn tissue distribution). Reviewing the literature, it seems that only a molar histidine/zinc ration of 2,000 or higher will cause zinc deficiency.     

Effects of zinc supplementation on serum zinc and leptin levels,BMI, and body composition in hemodialysis patients

ProjectThe aim of this study was to determine the effects of zinc supplementation on serum zinc and leptin levels as well as on anthropometric status and some biochemical parameters in hemodialysis (HD) patients.ProcedureIn this randomized, double-blind, and placebo-controlled trial, sixty HD patients were randomly divided into groups to receive a daily supplement of 100 mg elemental Zn (supplemented group) or placebo (control group) for 60 days. Anthropometric measurements were taken using standard calibrated instruments. Serum zinc and leptin levels were determined by atomic absorption and ELISA method respectively before and after intervention.ResultsZinc supplementation resulted in significant increase in the mean serum zinc level in the experimental group while changes observed in the placebo group were not significant. The mean serum leptin in women part of the experimental group was decreased significantly after supplementation. After adjusting for age, BMI, body fat (%), serum zinc and dietary Zn intake, a negative and significant association was observed between serum zinc and leptin levels in all subjects (β = −0.33, P = 0.03) as a result of Zn supplementation.ConclusionsMore studies are needed to clarify the mechanisms by which serum leptin level is influenced as a result of zinc supplementation in HD patients.     

Zinc transport by transferrin in rat portal blood plasma.

Zinc transport in mesenteric lymph and zinc distribution in portal plasma and venous plasma were examined in rats that had been given an oral dose of ⁶⁵Zn. Less than 1% of an oral dose of ⁶⁵Zn appeared in the mesenteric lymph over a period of 8 hr. In portal plasma, approximately 70% of the isotope recovered after gel-filtration chromatography was bound to a protein that was identified as transferrin on the basis of molecular weight and electrophoretic properties. In venous plasma, the major fraction of ⁶⁵Zn was bound to albumin while the remainder of the isotope was associated with higher molecular weight proteins including transferrin and α₂-macroglobulins. These results demonstrate that zinc is transported from the intestine to the liver via the portal blood, and the results demonstrate that zinc is transported in portal plasma bound to transferrin.     

Protective role of zinc in liver damage in experimental diabetes demonstrated via different biochemical parameters

Diabetes mellitus is a serious worldwide metabolic disease, which is accompanied by hyperglycaemia and affects all organs and body system. Zinc (Zn) is a basic cofactor for many enzymes, which also plays an important role in stabilising the structure of insulin. Liver is the most important target organ after pancreas in diabetic complications. In this study, we aimed to investigate the protective role of Zn in liver damage in streptozotocin (STZ)‐induced diabetes mellitus. There are four experimental groups of female Swiss albino rats: group I: control; group II: control + ZnSO₄; group III: STZ‐induced diabetic animals and group IV: STZ‐diabetic + ZnSO₄. To induce diabetes, STZ was injected intraperitoneally (65 mg/kg). ZnSO₄ (100 mg/kg) was given daily to groups II and IV by gavage for 60 days. At the end of the experiment, rats were killed under anaesthesia and liver tissues were collected. In the diabetic group, hexose, hexosamine, fucose, sialic acid levels, arginase, adenosine deaminase, tissue factor activities and protein carbonyl levels increased, whereas catalase, superoxide dismutase, glutathione‐S‐transferase, glutathione peroxidase, glutathione reductase and Na⁺/K⁺‐ATPase activities decreased. The administration of Zn to the diabetic group reversed all the negative effects/activities. According to these results, we can suggest that Zn has a protective role against STZ‐induced diabetic liver damage.     

Zinc-selenium interaction in the rat

Retention, dynamics of⁷⁵Se and⁶⁵Zn distribution, and elimination were studied in rats after separate or joint single doses of these metals. White female Wistar rats were divided into four groups (fifteen rats each). Group I received Na₂ ⁷⁵SeO₃ (0.1 mg Se/kg i.g.), group II received Na₂ ⁷⁵SeO₃+ZnCl₂ (5 mg Zn/kg s.c.), group III received⁶⁵ZnCl₂, and group IV received⁶⁵ZnCl₂+Na₂SeO₃. The zinc and selenium contents in the tissues were estimated during 120 h after administration; excretion in urine and feces of animals was determined throughout the experiment. Combined administration of zinc and selenium resulted in an enhanced selenium retention in the brain, spleen, kidneys, blood, lungs, and heart. A selenium-induced increase in the concentration of zinc was noted in the bowels, blood, liver, kidneys, spleen, brain, and lungs. The effects of the zinc/selenium interaction were visible especially in the lowered level of excretion of these elements. Zinc induced a decrease in the excretion of selenium in urine, with no concomitant changes in the excretion in feces. However, a visible decrease in the excretion of zinc in the feces was observed in the presence of selenium. The present results indicate an occurrence of clear-cut interaction effects between zinc and selenium administered simultaneously in the rat.     

<Superscript>153</Superscript>Sm and <Superscript>166</Superscript>Ho complexes with tetraaza macrocycles containing pyridine and methylcarboxylate or methylphosphonate pendant arms

A set of tetraaza macrocycles containing pyridine and methylcarboxylate (ac₃py14) or methylphosphonate (MeP₂py14 and P₃py14) pendant arms were prepared and their stability constants with La³⁺, Sm³⁺, Gd³⁺ and Ho³⁺ determined by potentiometry at 25 °C and 0.10 M ionic strength in NMe₄NO₃. The metal:ligand ratio for ¹⁵³Sm and ¹⁶⁶Ho and for ac₃py14, MeP₂py14 and P₃py14, as well as the pH of the reaction mixtures, were optimized to achieve a chelation efficiency higher than 98%. These radiocomplexes are hydrophilic and have a significant plasmatic protein binding. In vitro stability was studied in physiological solutions and in human serum. All complexes are stable in saline and PBS, but 20% of radiochemical impurities were detected after 24 h of incubation in serum. Biodistribution studies in mice indicated a slow rate of clearance from blood and muscle, a high and rapid liver uptake and a very slow rate of total radioactivity excretion. Some bone uptake was observed for complexes with MeP₂py14 and P₃py14, which was enhanced with time and the number of methylphosphonate groups. This biological profile supports the in vitro instability found in serum and is consistent with the thermodynamic stability constants found for these complexes.     

Copper binding components of blood plasma and organs,and their responses to influx of large doses of <Superscript>65</Superscript>Cu,in the mouse

To establish for the first time how mice might differ from rats and humans in terms of copper transport, excretion, and copper binding proteins, plasma and organ cytosols from adult female C57CL6 mice were fractionated and analyzed by directly coupled size exclusion HPLC-ICP-MS, before and after i.p. injection of large doses of ⁶⁵Cu. Plasma from untreated mice had different proportions of Cu associated with transcuprein/macroglobulin, ceruloplasmin and albumin than in humans and rats, and two previously undetected copper peaks (Mr 700 k and 15 k) were observed. Cytosols had Cu peaks seen previously in rat liver (Mr > 1000 k, 45 k and 11 k) plus one of 110 kDa. ⁶⁵Cu (141 μg) administered over 14 h, initially loaded plasma albumin and mainly entered liver and kidney (especially 28 kDa and 11 kDa components). Components of other organs were less (but still significantly) enriched. ⁶³Cu/⁶⁵Cu ratios returned almost to normal by 14 days, indicating a robust system for excreting excess copper. We conclude that there are significant differences but also strong similarities in copper metabolism between mice, rats and humans; that the liver is able to buffer enormous changes in copper status; and that a large number of mammalian copper proteins remain to be identified.     

Enhanced [<Superscript>3</Superscript>H] Glutamate Binding in the Cerebellum of Insulin-Induced Hypoglycaemic and Streptozotocin-Induced Diabetic Rats

Aim Energy deprivation causes neuronal death affecting the cognitive and memory ability of an individual. The kinetic parameters of glutamate dehydrogenase (GDH), the enzyme involved in the production of glutamate, was studied in the cerebellum and liver and the binding parameters of glutamate receptors in the cerebellum of insulin-induced hypoglycaemic and streptozotocin-induced diabetic rats were studied to reveal the role of glutamate excitotoxicity. Methods A single intrafemoral dose of streptozotocin was administered to induce diabetes. Hypoglycaemia was induced by appropriate doses of insulin subcutaneously in control and diabetic rats. The kinetic parameters V _max and K _m of GDH were studied spectrophotometrically at different substrate concentrations of α-ketoglutarate. Glutamate receptor binding assay was done with different concentrations of [³H] Glutamate. Results The GDH enzyme assay showed a significant increase (P < 0.001) in the V _max of the enzyme in the cerebellum of hypoglycaemic and diabetic rat groups when compared to control. The V _max of hypoglycaemic groups was significantly increased (P < 0.001) when compared to diabetic group. In the liver, the V _max of GDH was significantly increased (P < 0.001) in the diabetic and diabetic hypoglycaemia group when compared to control. The V _max of GDH increased significantly (P < 0.001) in the diabetic hypoglycaemic rats compared to diabetic group, whereas the control hypoglycaemic rats showed a significant decrease in V _max (P < 0.001) when compared to diabetic and diabetic hypoglycaemic rats. The K _m showed no significant change amongst the groups in cerebellum and liver. Scatchard analysis showed a significant increase (P < 0.001) in B _max in the cerebellum of hypoglycaemic and diabetic rats when compared to control. The B _max of hypoglycaemic rats significantly increased (P < 0.001) when compared to diabetic group. In hypoglycaemic groups, B _max of the control hypoglycaemic rats showed a significant increase (P < 0.001) compared to diabetic hypoglycaemic rats. The K _d of the diabetic group decreased significantly (P < 0.01) when compared to control and control hypoglycaemic rats. There was a significant decrease (P < 0.05) in the K _d of diabetic hypoglycaemic group when compared to the control hypoglycaemic rats. Conclusion Our studies demonstrated the increased enzyme activity in the hypoglycaemic rats with increased production of extracellular glutamate. The present study also revealed increased binding parameters of glutamate receptors reflecting an increased receptor number with increase in the affinity. This increased number of receptors and the increased glutamate production will lead to glutamate excitotoxicity and neuronal degeneration which has an impact on the cognitive and memory ability. This has immense clinical significance in the management of diabetes and insulin therapy.     

Biosorption of Pb<Superscript>2+</Superscript> and Zn<Superscript>2+</Superscript> by Non-Living Biomass of <Emphasis Type="Italic">Spirulina</Emphasis> sp.

Removal of heavy metals (Pb²⁺, Zn²⁺) from aqueous solution by dried biomass of Spirulina sp. was investigated. Spirulina rapidly adsorbed appreciable amount of lead and zinc from the aqueous solutions within 15 min of initial contact with the metal solution and exhibited high sequestration of lead and zinc at low equilibrium concentrations. The specific adsorption of both Pb²⁺ and Zn²⁺ increased at low concentration and decreased when biomass concentration exceeded 0.1 g l⁻¹. The binding of lead followed Freundlich model of kinetics where as zinc supported Langmuir isotherm for adsorption with their r ² values of 0.9659 and 0.8723 respectively. The adsorption was strongly pH dependent as the maximum lead biosorption occurred at pH 4 and 10 whereas Zn²⁺ adsorption was at pH 8 and 10.