Effect of NaF on Rat Parotid Gland Amylase Activity and cAMP Concentration in vitro and in vivo

Shahed, Asha; Bondi, J.; Allmann, David W.

doi:10.1177/00220345850640090501

Cited by 9 publications

(7 citation statements)

References 19 publications

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“…Due to the similarities between the effect of NaF and isoproterenol on parotid gland cells, it is speculated that NaF, by activating cAMP-dPK activity, may also phosphorylate proteins which play a regulatory role in amylase secretion. In addition, the present results support the suggestion made previously by Shahed et al (1985), that, under in vivo conditions, NaF induces amylase secretion by a cAMP-mediated mechanism.…”

Section: Resultssupporting

confidence: 93%

“…The pellet was homogenized and assayed for cAMP-dPK activity in the presence and absence of cAMP (see "Methods"). We have previously reported that NaF increased cAMP levels in, and amylase secretion from, rat parotid gland slices and that a single injection of NaF (15 mg F/kg) to rats decreased amylase content and increased cAMP level in rat parotid glands (Shahed et al, 1985). Since the results of whole animal studies 0 5 10 20 and, to a certain extent, tissue slices are difficult to interpret, due to the potential involvement of hormonal and/or neural effects, the present studies were conducted to investigate the mechanism of NaF-induced amylase secretion by isolated parotid gland cells.…”

Section: Resultsmentioning

confidence: 88%

“…In addition, NaF reportedly alters several cellular functions, e.g., carbohydrate metabolism in rat hepatocytes (Shahed et al, 1979a), histamine release from mast cells (Patkar et al, 1977;Alm, 1983), serotonin and nucleotide release from human blood platelets (Mirer and Daniel, 1983), granulocyte function (Elferink et al, 1982), and superoxide formation in polymorphonuclear leukocytes (Elferink, 1981;Sbarra and Karnovsky, 1959;Gabler et al, 1986), and increases gastric H+ secretion (Assem and Wan, 1982;Shayiq et al, 1984). We have previously reported that a single acute dose of NaF increased cAMP concentration and decreased amylase content in rat parotid glands (Shahed et al, 1985). The aim of the present study was to investigate the mechanism of NaF-stimulated amylase secretion in parotid gland cells.…”

Section: )mentioning

confidence: 87%

“…Fluoride ion is a known activator of adenylate cyclase activity in vitro from virtually all tissues (Perkins, 1973) and has been shown to increase cAMP accumulation in isolated rat hepatocytes (Shahed et al, 1979b;Crooke et al, 1980) and in vivo in several rat tissues (Allmann and Kleiner, 1980;Boros et al, 1984;Shahed et al, 1985) and rabbit tissues (Singh and Susheela, 1982). In addition, NaF reportedly alters several cellular functions, e.g., carbohydrate metabolism in rat hepatocytes (Shahed et al, 1979a), histamine release from mast cells (Patkar et al, 1977;Alm, 1983), serotonin and nucleotide release from human blood platelets (Mirer and Daniel, 1983), granulocyte function (Elferink et al, 1982), and superoxide formation in polymorphonuclear leukocytes (Elferink, 1981;Sbarra and Karnovsky, 1959;Gabler et al, 1986), and increases gastric H+ secretion (Assem and Wan, 1982;Shayiq et al, 1984).…”

Section: )mentioning

confidence: 99%

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Effect of NaF on cAMP Accumulation, cAMP-dependent Protein Kinase Activity in, and Amylase Secretion from, Rat Parotid Gland Cells

Shahed

Allmann

1988

J Dent Res

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Stimulation of amylase secretion from parotid glands by beta-adrenergic agonists is mediated by the activation of adenylate cyclase and the resultant increase in cellular cAMP. Since NaF is known to increase adenylate cyclase activity and cAMP accumulation in intact cells, we investigated whether it would stimulate amylase secretion from isolated rat parotid gland cells. The results provide evidence that the addition of NaF (0.01-10 mmol/L) increased cAMP concentration (1.5-2.8-fold) in, and amylase secretion (16-93%) from, isolated parotid gland acinar cells. NaF was found to increase cAMP-dependent protein kinase activity ratios (51-84%) in a concentration- and time-dependent manner. The data suggest that the stimulation of amylase secretion from parotid gland cells by NaF may be mediated by an increase in the cellular cAMP concentration, which exerts its effect, at least in part, by increasing the activity of cAMP-dependent protein kinase.

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Section: Resultssupporting

confidence: 93%

Section: Resultsmentioning

confidence: 88%

Section: )mentioning

confidence: 87%

Section: )mentioning

confidence: 99%

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Effect of NaF on cAMP Accumulation, cAMP-dependent Protein Kinase Activity in, and Amylase Secretion from, Rat Parotid Gland Cells

Shahed

Allmann

1988

J Dent Res

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“…A dose de 15 mg F -/kg p.c. é considerada relativamente alta e subtóxica e foi escolhida por demonstrar, em estudos anteriores com ratos, o aumento nas concentrações de AMPc após 30 e 60 minutos nas glândulas submandibulares (ALLMANN; KLEINER, 1980); redução da atividade da α-amilase em glândula parótida (SHAHED; BONDI; ALLMANN, 1985), além de, hiperglicemia (ALLMANN;KLEINER, 1980). Os valores da DL 50 estabelecidos para ratos machos tratados com NaF, via i.p., variam de 85,5 a 98,0 mg F -/kg (WHITFORD, 1989).…”

Section: Análise Estatísticaunclassified

Estudo da administração de flúor e o estresse oxidativo em glândulas salivares de ratos

Yamaguti¹

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Fluoride (F) is a toxicological axiom. Many reports have proposed that in varying concentrations, F induces increased reactive oxygen species generation, enhanced lipid peroxidation and impairs the antioxidant enzyme defence system in blood and tissues of experimental animals causing several biochemical alterations. Although the most pronounced effects of F intake are manifested in bones and teeth, soft tissues are also affected. Due to the paucity of reports investigating the short-and long-term effects of varied doses of F on soft tissues, especially salivary glands, this study aimed to evaluate the acute and long-term effects of sodium fluoride (NaF) exposure on antioxidant enzyme defence system and lipid peroxidation in the submandibular (SM) and parotid (PA) salivary glands of rats. For the acute investigation, the experimental groups of rats were injected intraperitoneally with NaF solution (15 mg F-/kg b.w.), while control groups were administered the same volume of sodium chloride solution (0,9%). The animals were euthanized in groups 1, 3, 6, 12 and 24 hours after injection. To evaluate long-term exposure effects, experimental groups of rats were administered 100 pmm Fin their drinking water for 30, 60 and 90 days. The control groups were provided with untreated tap water over the same periods. In all groups, after euthanization the SM and PA glands of each rat were extracted and analyzed for superoxide dismutase (SOD) and catalase (CAT) activities, malondialdehyde (MDA), protein and blood glycemia content. For both acute and long-term experiments, the experimental groups demonstrated higher levels of glycemia, altered levels of SOD and CAT in both glands, and increased levels of MDA in blood and salivary tissues of both glands. There were no differences in protein content for the acute experiment, but in the long-term experiment, increased protein levels were observed after 90 days in the SM gland and decreased protein levels were observed in the PA gland after 30 and 60 days. These results suggest that F impaired the antioxidant defence system and enhanced the levels of MDA in blood and SM and PA salivary glands of rats.

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Fluoride mediates apoptosis in osteosarcoma UMR 106 and its cytotoxicity depends on the pH

Hirano

Ando

1997

Archives of Toxicology

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Although an excess intake of fluoride has been reported to cause skeletal fluorosis, very little is known about the mechanism of adverse effects of fluoride on bone. In the present study cytotoxic effects of fluoride were studied using the osteosarcoma cell line, UMR 106. The DNA ladder formation upon agarose electrophoresis and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) staining revealed that UMR 106 underwent apoptosis following exposure to 5 mM fluoride for 8 h. On the other hand exposure to A23187, a calcium ionophore, caused necrosis while co-exposure to fluoride and A23187 inhibited fluoride-mediated apoptosis in UMR 106. The proliferation of UMR 106 cells cultured for 6 days in the presence of 0.5 mM fluoride was significantly decreased compared to the control culture. The cytotoxic effects of fluoride were modulated by both the cell density and the pH of the culture medium. The fluoride-induced viability loss in UMR 106 was enhanced in culture of high cell-density and inversely correlated with pH of the culture medium. Enhancement of fluoride cytotoxicity at acidic pH was also observed in rat alveolar macrophages and RAW 264, a macrophage cell line. The results suggest that fluoride-mediated apoptosis and culture conditions, including pH of the medium, should be taken into consideration to evaluate toxicity of fluoride in vitro.

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Effect of NaF on Rat Parotid Gland Amylase Activity and cAMP Concentration in vitro and in vivo

Cited by 9 publications

References 19 publications

Effect of NaF on cAMP Accumulation, cAMP-dependent Protein Kinase Activity in, and Amylase Secretion from, Rat Parotid Gland Cells

Effect of NaF on cAMP Accumulation, cAMP-dependent Protein Kinase Activity in, and Amylase Secretion from, Rat Parotid Gland Cells

Estudo da administração de flúor e o estresse oxidativo em glândulas salivares de ratos

Fluoride mediates apoptosis in osteosarcoma UMR 106 and its cytotoxicity depends on the pH

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