大气SO2、氟化物对植物生理生态指标的影响

运用多元回归分析方法研究不同污染区生长的植物叶片的生理生态指标的变化与大气硫酸盐化速率及氟化物浓度的关系.结果表明,植物的叶面积(LA)、叶绿素总量(Chl)、细胞液pH值(pH)和细胞质膜透性(CML电导率)等生理生态指标的变化幅度与大气污染物含量呈显著相关.与大气硫酸盐化速率关系式为Ys=0.034XLA-0.011XChl+0.017XpH+40.0003XCML+0.034(r=0.99,p＜0.001);与大气氟化物含量的关系式为YF=0.362XLA+0.329XChl+0.814XpH+0.024XCML-4.596(r=0.947,p＜0.03).利用这些生理生态指标的变化幅度作为生物监测的指标来评价不同污染区的大气硫氧化物、氟化物的污染状况,与大气监测结果有很高的一致性,并且与实际环境污染状况相符.     

Renal adaptive response to exposure to low doses of uranyl nitrate and sodium fluoride in mice

BackgroundDespite their differences in physicochemical properties, both uranium (U) and fluoride (F) are nephrotoxicants at high doses but their adverse effects at low doses are still the subject of debate. METHODS: This study aims to improve the knowledge of the biological mechanisms involved through an adaptive response model of C57BL/6 J mice chronically exposed to low priming doses of U (0, 10, 20 and 40 mg/L) or F (0, 15, 30 and 50 mg/L) and then challenged with acute exposure of 5 mg/kg U or 7.5 mg/kg NaF.ResultsWe showed that an adaptive response occurred with priming exposures to 20 mg/L U and 50 mg/L F, with decreased levels of the biomarkers KIM-1 and CLU compared to those in animals that received the challenge dose only (positive control). The adaptive mechanisms involved a decrease in caspase 3/7 activities in animals exposed to 20 mg/L U and a decrease in in situ VCAM expression in mice exposed to 50 mg/L F. However, autophagy and the UPR were induced independently of priming exposure to U or F and could not be identified as adaptive mechanisms to U or F.ConclusionTaken together, these results allow us to identify renal adaptive responses to U and F at doses of 20 and 50 mg/L, probably through decrease apoptosis and inflammatory cell recruitment.     

Establishment of drug delivery system nanocapsulated with an antioxidant (+)-catechin hydrate and sodium meta borate chelator against sodium fluoride induced oxidative stress in rats

Oxidative stress a major cause of fluoride induced toxicity and mitochondrial impairment in common in experimental rats during chronic exposure of fluoride. Attempts have been made in the present experiment to diminish oxidative damage, combined therapy with (+)-catechin hydrate (an antioxidant) and sodium meta borate (chelator) were used. Fluoride intoxication in rats was performed by using 13 mg/kg NaF and both antioxidant CH and chelator SMB were used at a concentration of 8.98 μM/kg body weight. Mixture of CH and SMB in free or in PLGA nanocapsule encapsulated form were prepared. The efficacies of those formulations were tested in combating free radical mediated oxidative insult produced by sodium fluoride (NaF). The amalgamated therapy used in this experiment was shown to reduce fluoride levels in liver, brain and kidney from 9.5, 5.5, 6.3 μg/g to 4.6, 2, 2.6 μg/g, respectively. Our result indicated that the combined chelator and antioxidant therapy in nanocapsulated drug delivery system could provide a projection in combating fluoride induced mitochondrial impairment in rat model.     

Fluoride and beryllium interact with the (Na + K)-dependent ATPase as analogs of phosphate

Fluoride irreversibly inhibits the (Na + K)-ATPase, and this inactivation requires divalent cations (Mg²⁺, Mn²⁺, or Ca²⁺), is augmented by K⁺, but is diminished by Na⁺ and by ATP. Prior incubation with the aluminum chelator deferoxamine markedly slows inactivation, whereas adding 1 µM AlCl₃ speeds it, consistent with AlF _– ⁴ being the active species. Prior incubation of the enzyme with vanadate also blocks inactivation by fluoride added subsequently. Fluoride stimulates ouabain binding to the enzyme, and thus the analogy between AlF _– ⁴ and both orthophosphate and orthovanadate is reflected not only in the similar dependence on specific ligands for their enzyme interactions and their apparent competition for the same sites, but also in their common ability to promote ouabain binding. Beryllium also irreversibly inhibits the enzyme, and this inactivation again requires divalent cations, is augmented by K⁺, but is diminished by Na⁺ and by ATP. Similarly, prior incubation of the enzyme with vanadate blocks inactivation by beryllium added subsequently. Inactivation by beryllium, however, does not require a halide, and, unlike inactivation by fluoride, increases at basic pHs. These observations suggest that beryllium, as beryllium hydroxide complexes, acts as a phosphate analog, similar to AlF _– ⁴ and vanadate.Abbreviations EDTA ethylenediaminetetraacetate - EGTA Ethyleneglycol-bis(-aminoethylether)-N,N-tetraacetate - FITC fluorescein isothiocyanate - HEPES N-2-hydroxyethylpiperazine-N-2-ethanesulfonic acid - PIPES piperazine-N,N-bis(2-ethanesulfonic acid)1,4-piperazine diethanesulfonic acid     

Fluoride profiles in the cementum and root dentine of human permanent anterior teeth extracted from adult residents in a naturally fluoridated and a non-fluoridated area

Objectives: To determine the effect of water fluoride concentration on the fluoride profile across the entire thickness of the cementum and root dentine of human permanent anterior teeth in adults. Subjects: Twenty-eight human permanent anterior teeth from individuals aged from 30 to over 60 years were studied. Setting: Teeth were obtained from a natural high-fluoride area (West Hartlepool, UK; 1.0–1.3 ppm F in drinking water, WHP) and the other from a non-fluoridated naturally low fluoride area (Leeds, UK; 0.1 ppm F in drinking water, LDS). Design: Cementum and root dentine were sampled using an abrasive micro-sampling technique from the cementum surface to the pulpal surface of root dentine. Results: Fluoride concentration was higher in tooth roots (the cementum and dentine) taken from the naturally fluoridated area (WHP) than from the non-fluoridated area (LDS). Age and average fluoride concentration showed a positive correlation in WHP dentine, middle region of the root (r = 0.78, P < 0.001) and in the apical region of the root (r = 0.67, P < 0.05). WHP cementum had the strongest fluoride concentration correlation with age in the cervical region of the root (r = 0.67, P < 0.01). An analysis of variance (ANOVA) showed that the area (water fluoride content), age and number of years lived in the area combined with total age were significant. Conclusions : The fluoride content of cementum and root dentine in adult residents is related to fluoride content in drinking water.     

氟污染区绿化树种的选择

前言凡使用含氟矿石(如冰晶石、磷矿石等)作原料的工厂,在碾磨、加热、酸化等过程中,以及利用含氟化合物作为接触剂、助熔剂的各种工艺过程的生产中,都会散发出大量的含氟废气与粉尘污染环境,给农林业生产及人     

Effects of fluoride on hepatic antioxidant system and transcription of Cu/Zn SOD gene in young pigs

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.     

Fluoride-Induced Oxidative Stress in Rat’s Brain and Its Amelioration by Buffalo (<Emphasis Type="Italic">Bubalus bubalis</Emphasis>) Pineal Proteins and Melatonin

Fluoride (F) becomes toxic at higher doses and induces some adverse effects on various organs, including brain. The mechanisms underlying the neurotoxicity caused by excess fluoride still remain unknown. The aims of this study were to examine F-induced oxidative stress (OS) and role of melatonin (MEL) and buffalo pineal proteins (PP) against possible F-induced OS in brain of rats. The 24 rats were taken in present study and were divided into four groups: control, F, F + PP, and F + MEL. The F group was given 150 mg/L orally for 28 days. Combined 150 ppm F and 100 μg/kg BW (i.p.) PP and F (150 ppm) + MEL (10 mg/kg BW, i.p.) were also administered. The activities of enzymatic, viz., superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), glutathione reductase (GR), and non-enzymatic, viz., reduced glutathione (GSH) concentration, and the levels of malondialdehyde (MDA) in the brain tissue were measured to assess the OS. Fluoride administration significantly increased brain MDA compared with control group, while GSH levels were decreased in fluoride-treated groups, accompanied by the markedly reduced SOD, GPx, GR, and SOD activity. Buffalo PP and MEL administration caused brain MDA to decrease but caused SOD, GPx, GR, GSH, and CAT activities to increase to significant levels in F-treated animals. Together, our data provide direct evidence that buffalo PP and MEL may protect fluoride-induced OS in brain of rats through mechanisms involving enhancement of enzymatic and non-enzymatic antioxidant defense system. Therefore, this study suggested that PP and MEL can be useful in control of neurotoxicity induced by fluoride.     

Ultrastructural morphometric analysis of ameloblasts exposed to fluoride during tooth development

Since a considerable amount of the world population is exposed to high doses of fluoride, it is of special concern to investigate its action mechanisms during dental enamel development. In this study, the toxicity of fluoride in ameloblasts during enamel development was evaluated by means of ultrastructural morphometric analysis. A total of 18 male Wistar rats were distributed into three groups. In Group I, the animals received deionized drinking water ad libitum (negative control) and in Groups II and III, they received sodium fluorided (NaF) drinking water at doses of 7 and 100 ppm ad libitum, respectively, for 6 weeks. Morphometric data were expressed as volume density of the most significant organelles present in the secretory and maturation phases of amelogenesis such as RER, granules, lysosomes, phagic vacuoles, microfilaments and mitochondria. The results showed that the volume density of mitochondria in the 100 ppm experimental group was 29% (P < 0.05) higher than the control group in secretory ameloblasts. No remarkable differences were found in maturation ameloblasts for all organelles evaluated. Taken together, these data indicate that NaF at high doses is able to induce cellular damage in secretory ameloblasts, whereas no noxious effect was observed during maturation stage of amelogenesis as depicted by ultrastructural analysis.     

A fluoride-insensitive inorganic pyrophosphatase isolated from Methanothrix soehngenii

An inorganic pyrophosphatase [E.C. 3.6.1.1] was isolated from Methanothrix soehngenii. In three steps the enzyme was purified 400-fold to apparent homogeneity. The molecular mass estimated by gelfiltration was 139±7 kDa. Sodium dodecyl sulfate/polyacrylamide gel electrophoresis indicated that the enzyme is composed of subunits with molecular masses of 35 and 33 kDa in an _{2 2} oligomeric structure. The enzyme catalyzed the hydrolysis of inorganic pyrophosphate, tri-and tetrapolyphosphate, but no activity was observed with a variety of other phosphate esters. The cation Mg²⁺ was required for activity. The pH optimum was 8 at 1 mM PP _i and 5 mM Mg²⁺. The enzyme was heat-stable, insensitive to molecular oxygen and not inhibited by fluoride. Analysis of the kinetic properties revealed an apparent K _m for PP _i of 0.1 mM in the presence of 5 mM Mg²⁺. The V _max was 590 mol of pyrophosphate hydrolyzed per min per mg protein, which corresponds to a K _cat of 1400 per second.The enzyme was found in the soluble enzyme fraction after ultracentrifugation, when cells were disrupted by French Press. Upto 5% of the pyrophosphatase was associated with the membrane fraction, when gentle lysis procedyre were applied.Abbreviation PMSF phenylmethylsulfonyl fluoride