A new host record for Candidatus Phytoplasma cynodontis (16Sr XIV-A) associated with phyllody and fasciation of linseed (Linum usitatissimum) from India.

Linseed commonly called as flaxseed (Linum usitatissimum Linn.) is an important oilseed crop cultivated widely in Northern parts of Karnataka. During, 2019 (January-February), a characteristic disease was noticed with symptoms that resembled phytoplasma or like disease symptoms. The incidence was ranged from 6·5 to 16·5% in the experimental station of Raichur Agricultural University. The typical symptoms observed were virescence of floral parts, fasciation of the inflorescence axis, phyllody, stunted and flattened stem with reduced leaves. Symptomatic and healthy samples were collected and processed for molecular detection of phytoplasma. Total DNA was isolated from four infected plants and two healthy plants. The 16S rDNA region was amplified using P1/P7 followed by R16F2n/R16R2 primer pair which showed the amplification of expected amplicon size from all four infected samples. Furthermore, the SecA gene was amplified using SecA1/SecA3 primers. The PCR amplified products were subjected for direct sequencing from both directions and the consensus sequences were obtained and nBLAST search analysis revealed that the 16Sr RNA and SecA sequences were sharing maximum similarity (100%) with the reference sequence of Ca. P. cynodontis. The sequences were analysed phylogenetically by constructing a Phylogram independently by NJ method along with reference sequence of 16S rRNA region and SecA region retrieved from GenBank database showed that the phytoplasma sequence from linseed phyllody of the present study placed in a distinct clade along with reference sequence of "Ca. P. cynodontis" thus confirming the identity phylogenetically. Furthermore, iPhyClassifier and virtual RFLP proved that the phytoplasma belonged to 16SrXIV (subgroup A) phytoplasma. Previously linseed is known to be associated with 16SrII-D phytoplasma but the association of the 16SrXIV-A group of phytoplasma is not reported so far. Therefore, this is the new host record for Ca. P. cynodontis (16SrXIV-A) phytoplasma associated with linseed stem fasciation, phyllody from India.

Protective effect of Allium sativum (garlic) aqueous extract against lead-induced oxidative stress in the rat brain, liver, and kidney.

The present investigation was undertaken to evaluate the ameliorative activity of Allium sativum against lead-induced oxidative stress in the brain, liver, and kidney of male rats. Four groups of male Wistar strain rats (100-120 g) were taken: group 1 received 1000 mg/L sodium acetate and group 2 was given 1000 mg/L lead acetate through drinking water for 2 weeks. Group 3 and 4 were treated with 250 mg/kg body weight/day of A. sativum and 500 mg/kg body weight/day of A. sativum, respectively, by oral intubation for a period of 2 weeks along with lead acetate. The rats were sacrificed after treatment and the brain, liver, and kidney were isolated on ice. In the brain, four important regions namely the hippocampus, cerebellum, cerebral cortex, and brain stem were separated and used for the present investigation. Blood was also drawn by cardiac puncture and preserved in heparinized vials at 4 °C for estimation of delta-aminolevulinic acid dehydratase (ALAD) activity. The results showed a significant (p < 0.05) increase in reactive oxygen species (ROS), lipid peroxidation products (LPP), total protein carbonyl content (TPCC), and lead in the selected brain regions, liver, and kidney of lead-exposed group compared with their respective controls. Blood delta-ALAD activity showed a significant (p < 0.05) decrease in the lead-exposed rats. However, the concomitant administration of A. sativum resulted in tissue-specific recovery of oxidative stress parameters namely ROS, LPP, and TPCC. A. sativum treatment also restored the blood delta-ALAD activity back to control. Overall, our results indicate that A. sativum administration could be an effective antioxidant treatment strategy for lead-induced oxidative insult.

Macrobenthos response to sewage pollution in a tropical inshore area.

Organic sewage pollution is the major stressor that affects benthic communities in the coastal waters. In the present study involving a once-off sampling (July-August 2003) of a sewage treatment plant (STP) outfall and areas 6 km farther into the sea, we tried to estimate the severity of organic pollution on marine macrobenthos over a pollution gradient in the inshore waters (station depths, 5-30 m) off a heavily urbanized tropical city, on the east coast of India. Multivariate ordination analyses revealed two different groups of faunal assemblages. Group I is associated with sites impacted by the sewage outfall and group II with the locations 3-6 km away in the open sea. Polychaetes and amphipods were the predominant fauna with significant taxonomic differences between the assemblages. Despite the homogeneity in sediment texture, the two-fold increase in sediment organic matter near the sewage outfall area supported r-strategists, while group II locations favoured K-strategists. Approximation through benthic opportunistic polychaetes amphipods (BOPA) index and information on the key taxa responsible for the observed assemblage patterns corroborated these findings. Thus, the present findings revealed how organic sewage pollution influences benthic diversity in coastal waters by supporting communities of opportunistic characteristics. We advocate inclusion of community traits and compatible analytical tools (statistical approaches) in studies of similar nature so that the observations could be compared and broad remedial measures could be evolved.

Pb2+ reduces PKCs and NF-kappaB in vitro.

The mechanism of lead (Pb(2+))-induced neurotoxicity has not yet been fully elucidated. The purpose of this study was to examine the effects of Pb(2+) on several protein kinase C (PKC) isoforms and the nuclear factor-kappaB (NF-kappaB)-I-kappaB kinase-alpha (IKK-alpha) axis in cultured neuronal cells. Neurons were isolated from rat fetal brain at the 18th day of gestation of pregnant Sprague Dawley rats and cultured for 10 days before use. Neurons were exposed to Pb(2+) at concentrations of 10(-10), 10(-9), 10(-8), and 10(-7) mol/L for 14 h and antigens of typical PKC-alpha,beta,gamma; novel PKC (epsilon, delta), atypical PKC (lambda), NF-kappaB (p50), and IKK-alpha were enriched by immunoprecipitation and determined by western blotting. Total, calcium-dependent and independent PKC activities were also determined by counting the transferred gamma-(32) P in the substrate-histone. The results indicated that inorganic Pb(2+) significantly reduced all PKC isoforms (alpha,beta,gamma, epsilon, lambda) except delta, inhibiting the total, calcium-dependent and calcium-independent PKC activities in a dose-dependent manner. Additionally, Pb(2+) gradually reduced NF-kappaB (p50) and IKK-alpha protein levels. This suggests that Pb(2+) exhibits varying preference for individual PKC isoforms but reduces the NF-kappaB-IKK-alpha axis to a similar extent.

Cadmium accumulation and detoxification by alveolar macrophages of cigarette smokers.

STUDY OBJECTIVES: Cadmium (Cd) is a toxic metal associated with emphysema and lung cancer, which is present in both air pollution and cigarette smoke. Metallothionein (MT) is an inducible protein that binds and detoxifies cellular Cd. The goals of this study were to determine whether increased concentrations of Cd are present in alveolar macrophages (AMs) of cigarette smokers (CSMs) and to determine whether MT accumulated in response to the presence of Cd. DESIGN: AMs were recovered by BAL from 10 healthy nonsmokers (NSMs) and 10 CSMs. The Cd content of the AMs was determined by inductively coupled plasma-mass spectrometry, and the MT content was determined using a Cd/hemoglobin radioassay (with (109)Cd). MEASUREMENTS: Cd was detected in AMs recovered from all subjects, with higher mean (+/- SEM) concentrations in CSMs compared with those in NSMs (3.4 +/- 0.5 vs 1.3 +/- 0.2 ng/10(6) cells; p < 0.005). There was a correlation between current smoking history (cigarettes per day) and the AM content of Cd (r = 0.74; p < 0.05). The mean AM content of MT was similar in NSMs (1.2 +/- 0.2 microg/10(7) cells) and CSMs (1.0 +/- 0.2 microg/10(7) cells). CONCLUSIONS: AMs in CSMs accumulate significant amounts of Cd without a concurrent increase in MT content, indicating greater saturation of MT. Increased Cd burden in alveolar cells could contribute to the development of lung diseases in CSMs.

Lead induced alterations in nitrite and nitrate levels in different regions of the rat brain.

Nitric oxide (NO) is a free radical synthesized by nitric oxide synthase (NOS) during the conversion of L-arginine to citrulline. Lead (Pb) affects neuronal functioning in the rat brain. Nitric oxide, a neuronal messenger has a short half life and converts immediately into nitrite and nitrate. The present study is designed to determine lead-induced alterations in NO production by measuring nitrite and nitrate in the cerebellum, the hippocampus, the frontal cortex and the brain stem of the rat brain. Male Sprague-Dawley rats were treated with lead acetate (5 and 15 mg/kg body wt.) by intraperitoneal injection. The control and experimental rats were sacrificed at the end of 7 and 14 days after treatment and different regions of the brain were isolated. Nitrite and nitrate (NOx) levels were estimated by the chemiluminescent method using the NOA 280 (Sievers). The data suggested dose-dependent and region-specific responses to lead. Both treatments of lead reduced NOx levels in the cerebellum and the hippocampus. However, the frontal cortex and the brain stem responded differently to Pb exposure. NOx levels in the frontal cortex were significantly increased in rats treated with low and high doses of Pb for 7 days but not in rats treated for 14 days, whereas in the brain stem, NOx levels were increased in a dose- and time-dependent manner. Although, the response was time-dependent, the variation between 7- and 14-day treatment was not clearly delineated. These results provide additional evidence that Pb exposure alters NO-production in rat brain leading to neuronal dysfunction.

Pioglitazone and metformin reverse insulin resistance induced by tumor necrosis factor-alpha in liver cells.

Tumor necrosis factor-alpha (TNF-alpha) has recently been implicated as a cause of insulin resistance (IR) in obesity and non-insulin dependent diabetes mellitus (NIDDM). To examine mechanisms involved, we induced IR induced IR in H-411 E cells with graded doses of TNF-alpha and measured the ability of insulin (INS) to stimulate both calmodulin (CaM) mRNA and glucose utilization. With TNF-alpha concentration at 1 ng/ml and 10(4) muU/ml INS, metformin 10 microM and pioglitazone 1.5 microM, reversed the IR induced by TNF-alpha restoring biologic response to 100% of INS effect alone. Furthermore, comparable results were obtained with glucose utilization/oxidation experiments in the H-411 E cells using glucose U-14C, trapping 14CO2 release in a hyamine filter and extracting 14C labelled lipids with Dole's reagent. In condusion, these data add scientific support for the use of both metformin and pioglitazone in treatment of IR in NIDDM patients and support a rationale for use of use of these drugs alone, and in conjuction with oral agents and/or INS treatment.

In vitro metal inhibition of N-methyl-D-aspartate specific glutamate receptor binding in neonatal and adult rat brain.

The in vitro effect of methyl mercury (MM) and lead (Pb) on N-methyl-D-aspartate (NMDA)-specific glutamate receptor binding in neonatal (10 days old) and adult rat brain was investigated. The cerebral cortex was isolated from the neonatal and adult male Sprague-Dawley rats and the synaptic plasma membranes were prepared to study the NMDA-specific glutamate receptor binding by using (3H)-glutamic acid. The metal salts such as methyl mercury chloride and lead acetate were used to study the effect of MM and Pb. Both MM and Pb significantly inhibited the receptor binding in neonatal and adult rat brain in a concentration-dependent manner. MM (IC50:0.95 +/- 0.08 microM) was more potent in inhibiting the receptor binding than Pb (IC50:60 +/- 7 microM) in neonatal rat brain. A similar high potency was observed for MM than Pb in adult rat brain but the IC50 values are very high (70 +/- 6 microM and 300 +/- 24 microM respectively) indicating less effect compared to neonatal brain. The data suggest that NMDA-receptor binding was more sensitive to MM and Pb in neonatal brain than in adult. MM was more effective than Pb because of its more lipophilicity.

Interaction of metals with muscarinic cholinoceptor and adrenoceptor binding, and agonist-stimulated inositol phospholipid hydrolysis in rat brain.

In vitro mercury (Hg) or lead (Pb) effectively inhibited the binding of 3H-quinuclidinyl-benzilate (QNB) (a muscarinic cholinoceptor antagonist) and 3H-prazosin (an alpha 1-adrenoceptor antagonist) to their receptors in cerebellar and cerebral cortex membranes in a concentration-dependent manner. Hg was more potent than Pb. When the rats were treated with Hg (5 mg/kg body wt) or Pb (25 mg/kg body wt) for 24 hr, a decrease in 3H-prazosin and an increase in 3H-QNB receptor binding were observed in cerebral cortex. There was no alteration in 3H-prazosin binding in cerebellum with the above treatment of metals, but 3H-QNB binding in cerebellum was significantly inhibited by Hg. However, both 3H-prazosin and 3H-QNB receptor bindings were significantly decreased in cerebellum of rats treated for 7 days with Hg (1 mg/kg body wt/day) or Pb (25 mg/ kg body wt/day). But in cerebral cortex of rats treated with these metals for 7 days, a decrease in 3H-prazosin and an increase in 3H-QNB receptor binding activities were noticed. There was a significant decrease in phospholipid content in cerebral cortex but not in cerebellum of rats treated with these metals for 7 days. At 100 microM concentration carbachol or acetylcholine or norepinephrine stimulated 3H-inositol incorporation and 3H-inositol phosphate (IP) formation in rat cerebral cortical slices. Hg or Pb in vitro though increased the agonist-stimulated 3H-inositol incorporation, 3H-IP formation was not significantly altered. The present investigation demonstrates the differential responses by alpha 1-adrenoceptor and muscarinic cholinoceptor in cerebellum and cerebral cortex of rat to in vitro and in vivo effects of Hg or Pb.

In vitro and in vivo effects of lead, methyl mercury and mercury on inositol 1,4,5-trisphosphate and 1,3,4,5-tetrakisphosphate receptor bindings in rat brain.

In vitro and in vivo effects of mercury (Hg), methyl mercury (MM) and lead (Pb) on [3H]inositol 1,4,5-trisphosphate (IP3) and [3H]inositol 1,3,4,5-tetrakisphosphate (IP4) receptor binding in the Sprague-Dawley rat brain cerebellar membranes were studied. In vitro studies indicate that binding of [3H]IP3 and [3H]IP4 to cerebellar membranes was inhibited by Hg while they were stimulated by MM or Pb in a concentration-dependent manner. MM was more potent (EC50 3.4 microM) than Pb (EC50 18.2 microM) in stimulating the [3H]IP3 receptor binding activity whereas Pb (IC50 30 microM) was more potent than MM (IC50 133 microM) in stimulating the [3H]IP4 receptor binding. When the rats were treated (i.p) with Hg (5 mg/kg body wt.) or MM (5 mg/kg body wt.) or Pb (25 mg/kg body wt.) for 3 or 24 h, no significant alterations in [3H]IP3 receptor binding were observed in cerebellum and cerebral cortex. But the above treatment of Pb or MM for 3 or 24 h to rats resulted in an increase of [3H]IP4 receptor binding in the membranes of cerebral cortex. However, the rats treated with Hg (1 mg/kg body wt./day) or Pb (25 mg/kg body wt./day) for 7 days did not show any alteration in binding of [3H]IP3 to its receptors in cerebellar membranes but an increase in this receptor binding was noticed with the treatment of MM (2.5 mg/kg body wt./day) for 7 days. The cerebellum and cerebral cortex of rats with the above treatment of MM or Pb for 7 days exhibited an increase in [3H]IP4 receptor binding. These in vitro and in vivo data suggest that alterations in inositol polyphosphate receptor binding by metals could result in alterations in intracellular calcium levels which may influence neuronal activity.

Inhibition of calcium transport by mercury salts in rat cerebellum and cerebral cortex in vitro.

The present investigation was initiated to study the differential effects of mercury salts on calcium pump activity of rat cerebellum and cerebral cortex in vitro. The calcium pump activity was studied by assaying calcium-adenosine triphosphatase (Ca(2+)-ATPase) in synaptic plasma membranes (SPMs) and microsomes of cerebellum and cerebral cortex in the presence of different micromolar concentrations of mercury and methylmercury. The 45Ca uptake in microsomes of cerebellum and cerebral cortex was also determined in the presence of both the salts of mercury. The SPMs and microsomes were prepared by differential centrifugation using a sucrose gradient (0.8/1.2 M). The Ca(2+)-ATPase activity was determined by estimating the inorganic phosphate. The 45Ca uptake was measured in microsomes by using 45CaCl2. Calcium-ATPase in SPMs was significantly inhibited by these two mercury salts in a concentration-dependent manner. In cerebellum and cortex, the IC50 values for mercuric chloride were 0.065 and 0.081 microM, respectively, whereas they were 0.354 and 0.384 microM for methylmercury chloride, indicating that mercuric chloride was more potent in inhibiting the plasma membrane Ca2+ extrusion process when compared to methylmercury chloride. As seen in SPMs, Ca(2+)-ATPase and 45Ca uptake in microsomes were also significantly inhibited in both cerebellum and cortex by mercury salts in a concentration-dependent manner, the effect being greater with mercuric chloride. These results indicate that both mercury and methylmercury inhibited the Ca2+ pumps located in SPMs and microsomes differentially, and to some extent the effects were also region specific.

Modulation of protein kinase C by heavy metals.

Protein kinase C (PKC) regulates a variety of intracellular and extracellular signals across the neuronal membrane. PKC requires calcium and phospholipid, particularly phosphatidylserine (PS) for its activation. The data indicates that mercury (Hg), lead (Pb) and methyl mercury (CH3Hg) in vitro inhibited the PKC activity at micromolar concentrations in a concentration-dependent manner with IC50 values of 1.5, 2.12 and 0.22 microM, respectively. The IC50 values indicate that CH3Hg was more potent in inhibiting the enzyme activity than Hg or Pb. The basal PKC activity was also inhibited by Pb or Hg. However, the PS-stimulated PKC activity was more sensitive to Pb or Hg than the basal enzyme. The phorbol ester binding to PKC was also found to be inhibited by micromolar concentrations of these metals in vitro. Hg and CH3Hg were more potent inhibitors of phorbol ester binding than Pb. Dithiothreitol (DTT), a dithiol, but not glutathione (GSH) a monothiol, protected the activities of both PS-stimulated and basal PKC from metal-inhibition in a concentration-dependent manner. The present study suggests that the dithiols but not monothiols effectively protect metal-inhibited activity of PKC in rat brain.

Lead alters inositol polyphosphate receptor activities: protection by ATP.

Receptor-mediated phosphoinositide signaling pathway which generates a variety of second messengers is regulated by intracellular free Ca2+ concentrations. Since toxic metal cations like Pb2+ are known to alter Ca(2+)-dependent processes, the present study was initiated to study the effects of Pb2+ on inositol 1,4,5-trisphosphate (InsP3) and inositol 1,3,4,5-tetrakisphosphate (InsP4) receptor binding and InsP3-mediated Ca(2+)-release. Rat cerebellar membrane and microsomal fractions were incubated with various concentrations of Pb2+ (0.01-100 microM). Pb2+ significantly stimulated [3H]-InsP3 and [3H]-InsP4 receptor binding (EC50 22.7 and 13.5 microM respectively) as a function of metal concentrations. However, InsP3-mediated Ca2+ release, determined by measuring the changes in fluorescence intensity of Fura-2, was significantly inhibited by varying concentrations of Pb2+. Re-uptake of Ca2+ into the microsomes was also inhibited by Pb2+. A significant inhibition of microsomal Ca(2+)-pump by micromolar concentration of Pb2+ was also observed. ATP at 5-1000 microM concentration range inhibited [3H]-InsP3 and [3H]-InsP4 binding to the specific receptors. [3H]-InsP4 receptor binding was more sensitive to ATP inhibition as compared to [3H]-InsP3 receptor binding. Furthermore, varying concentrations of ATP also inhibited Pb(2+)-mediated increase in [3H]-InsP3 and [3H]-InsP4 receptor binding. The kinetic analysis of ATP effect on Pb(2+)-stimulated [3H]-InsP4 receptor binding revealed non-competitive type of interaction. The results of the present study suggest that Pb2+ may be increasing the binding of [3H]-InsP3 and [3H]-InsP4 to the specific receptors by modulating the conformation of the receptor sites. ATP may be playing a protective role in Pb2+ induced alteration of the receptor sites.

In vitro interaction of heavy metals with ouabain receptors in rat brain microsomes.

This study investigates the influence of heavy metals on ouabain-binding in presence of thiol (sulfhydryl) compounds. The data on in vitro effects of mercury (Hg), lead (Pb) and cadmium (Cd) showed significant inhibition of 3H-ouabain binding to microsomal membrane in a concentration-dependent manner. Maximum inhibition of 3H-ouabain binding was observed at 1 microM for Hg and 100 microM each for Pb and Cd. Preincubation with monothiol (L-cysteine or glutathione) or dithiol (dithiothreitol) protected inhibition of 3H-ouabain binding to the membranes by Hg or Pb. Dithiol but not monothiols partially protected Cd-inhibition. The present data confirm that the heavy metals interact with ouabain receptors in a manner similar to SH-blocking agents and protection of metal-inhibited 3H-ouabain binding by thiol compounds is metal specific.

The effects of cadmium in vitro on adenosine triphosphatase system and protection by thiol reagents in rat brain microsomes.

Cadmium (Cd) inhibited the activities of Na(+)-K+ ATPase (IC50 = 5.0 x 10(-5) M), K(+)-p-nitrophenyl phosphatase (PNPPase) (IC50 = 4.0 x 10(-5) M) and 3H-ouabain binding (IC50 = 7.5 x 10(-5) M) in rat brain microsomes. Monothiols (cysteine but not glutathione and D-penicillamine) and dithiols (dimercaprol, dimercaptosuccinic acid and dithiothreitol) offered varied levels of protection against Cd-inhibition of Na(+)-K+ ATPase. Protection of Na(+)-K+ ATPase by these sulfhydryl (SH) agents was higher at 7.5 as compared to 8.5 pH. The present data suggest that Cd-inhibited Na(+)-K+ ATPase, by interfering with phosphorylation of enzyme molecule and dephosphorylation of the enzyme-phosphoryl complex and exerts a similar effect to that of SH-blocking agents.

Effects of lead on pH and temperature-dependent substrate-activation kinetics of ATPase system and its protection by thiol compounds in rat brain.

Lead (Pb) inhibited the activities of Na(+)-K+ ATPase (IC50 = 2.0 x 10(-6) M), K(+)-Para-Nitrophenyl phosphatase (PNPPase) (IC50 = 3.5 x 10(-6) M) and [3H]-ouabain binding (IC50 = 4.0 x 10(-5) M) in rat brain P2 fraction. A variable temperature or pH significantly elevated the inhibition of Na(+)-K+ ATPase by Pb in buffered acidic, neutral and alkaline pH ranges. Noncompetitive inhibition with respect to activation of Na(+)-K+ ATPase by ATP was indicated by a variation in Vmax values with no significant changes in Km values at any temperature studied. In the presence of Pb, for Na(+)-K+ ATPase at pH 6.5 and 8.5, Vmax was decreased with an increase in Km values suggesting a mixed type of inhibition. Sulfhydryl agents such as dithiothreitol (DTT) and cysteine (Cyst), but not glutathione (GSH) offered varied levels of protection against Pb-inhibition of Na(+)-K+ ATPase at pH 7.5 and 8.5. The present data suggest that inhibition of Na(+)-K+ ATPase by Pb is both temperature and pH-dependent. These results also indicate that Pb inhibited Na(+)-K+ ATPase by interfering with phosphorylation of enzyme molecule and dephosphorylation of the enzyme-phosphoryl complex and exerted an effect similar to that of SH-blocking agents.

Effects of lead on kinetics of 3H-dopamine uptake by rat brain synaptosomes.

The effects of lead on 3H-dopamine (3H-DA) uptake in rat brain synaptosomes were studied. Pb inhibited 3H-DA uptake in vitro and in vivo in a concentration-dependent manner. Altered pH versus 3H-DA uptake demonstrated comparable inhibition in buffered acidic, neutral, and alkaline pH ranges, and higher inhibition was observed in neutral pH. Kinetic studies of ATP activation of 3H-DA uptake indicated competitive inhibition by Pb. The inhibition of 3H-DA uptake followed the Na+ concentrations. The results indicate that the Pb inhibition of 3H-DA uptake is pH, ATP, and Na+ dependent.

Effects in vitro of mercury on rat brain Mg(++)-ATPase.

Mercuric chloride (Hg) in micromolar concentrations inhibited Mg(++)-dependent ATPase activity in rat brain microsomes. Inhibition was higher in oligomycin-sensitive (O.S.) than oligomycin-insensitive (O.I.) Mg(++)-ATPase. Hydrolysis of ATP with 15 and 50 micrograms of microsomal protein for 45 min without and with (2.10(-7M) Hg showed linear rates for 15-20 min. Altered pH vs activity demonstrated comparable inhibitions by Hg in buffered (neutral greater than acidic greater than basic) pH ranges. Inhibition of enzyme activity by Hg was found to be greater at 37 degrees C than at lower temperatures suggesting positive correlation trend. An uncompetitive inhibition with respect to the activation of Mg(++)-ATPase, O.S. Mg(++)-ATPase and O.I. Mg++ ATPase by ATP was indicated by a decrease in apparent Vmax and Km. Mg(++)-activation kinetic studies indicated that Hg causes uncompetitive inhibition of Mg(++)-ATPase and O.I. Mg(++)-ATPase and mixed inhibition of O.S. Mg(++)-ATPase. Inhibition was partially restored by repeated washings. These results indicate that the inhibition of microsomal Mg(++)-ATPase by Hg was pH, temperature, enzyme and Mg++ concentration dependent. Additionally, the data also suggest that O.S. compared to O.I. Mg(++)-ATPase is more sensitive to Hg toxicity.

Effects of cadmium and mercury on Na(+)-K+, ATPase and uptake of 3H-dopamine in rat brain synaptosomes.

Effects in vivo of cadmium (Cd), mercury (Hg) and methylmercury (CH3Hg) on Na(+)-K+ ATPase and uptake of 3H-dopamine (DA) in rat brain synaptosomes were studied. These heavy metals significantly inhibited the Na(+)-K+ ATPase activity in a dose-dependent manner. Similarly, inhibition of DA uptake by synaptosomes was also observed in rats treated with these metals. Intraperitoneal route of metal administration was found to be more effective than per os treatment. Mercuric compounds compared to Cd elicited a higher inhibition of Na(+)-K+ ATPase and DA uptake in rat brain synaptosomes.