Diverse actions of cadmium on the smooth muscle myosin phosphorylation system

Kostrzewska, Anna; Sobieszek, Apolinary

doi:10.1016/0014-5793(90)81419-o

Cited by 22 publications

(9 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The possibility still exists, however, that Cd interferes with the downstream cascade of cAMP-protein kinase A-dependent pathway. Kostrzewska and Sobieszek [45] reported that higher Cd concentrations inhibited the phosphorylation of myosin light-chain kinase in the smooth muscle myosin, suggesting that Cd interferes with the phosphorylation of protein kinases. An additional possibility is that the metal may directly affect transcription of P450 scc by interfering with the DNA binding zinc finger motif through the substitution of Cd 2ϩ for Zn 2ϩ [46].…”

Section: Discussionmentioning

confidence: 98%

Placental Endocrine Disruption Induced by Cadmium: Effects on P450 Cholesterol Side-Chain Cleavage and 3β-Hydroxysteroid Dehydrogenase Enzymes in Cultured Human Trophoblasts

Kawai

Swan

Green

et al. 2002

Biology of Reproduction

View full text Add to dashboard Cite

We previously suggested that cadmium (Cd), an environmental toxicant and constituent of tobacco smoke, inhibits progesterone secretion in cultured human placental trophoblasts by inhibiting low-density lipoprotein receptor mRNA expression. In the current study, we investigated whether Cd also disrupts progesterone synthesis via P450 cholesterol side-chain cleavage (P450(scc)) and 3beta-hydroxysteroid dehydrogenase (3beta-HSD), enzymes that play important roles in placental steroidogenesis. Human cytotrophoblasts were purified by density gradient centrifugation and incubated in Dulbecco modified Eagle medium + 10% fetal bovine serum with 0, 5, 10, or 20 microM CdCl(2) for 96 h. Cells progressed to syncytiotrophoblastic maturity regardless of treatment. No differences (P > 0.05) in cell protein and lactate dehydrogenase activity were observed between untreated trophoblasts and those treated with CdCl(2). However, P450(scc) and 3beta-HSD mRNA transcript levels declined in a dose-dependent manner (P <0.05) in trophoblasts cocultured with 5, 10, or 20 microM CdCl(2). P450(scc) activity was similarly inhibited (P < 0.05) by CdCl(2) treatment, although 3beta-HSD activity was not significantly affected. Coculture with 8-bromo-cAMP enhanced progesterone secretion in untreated cultures but did not reverse the decline in progesterone secretion induced by CdCl(2) treatment. CdCl(2) failed to influence cAMP content in cultured cells. Collectively, results suggest that P450(scc) enzyme is another site at which Cd interferes with placental progesterone production. However, it is unlikely that an inhibition of cAMP is involved with the inhibition of progesterone biosynthesis by Cd in human trophoblasts.

show abstract

Section: Discussionmentioning

confidence: 98%

Placental Endocrine Disruption Induced by Cadmium: Effects on P450 Cholesterol Side-Chain Cleavage and 3β-Hydroxysteroid Dehydrogenase Enzymes in Cultured Human Trophoblasts

Kawai

Swan

Green

et al. 2002

Biology of Reproduction

View full text Add to dashboard Cite

show abstract

“…Although Cd 2+ is best known as a Ca 2+ channel blocker, it can also activate calmodulin and have other effects as well (e.g., Kostrzewska and Sobieszek, 1990;Behra, 1993). …”

Section: Discussionmentioning

confidence: 99%

Two distinct, calcium-mediated, signal transduction pathways can trigger deflagellation in Chlamydomonas reinhardtii

Quarmby

Hartzell

1994

The Journal of Cell Biology

108

View full text Add to dashboard Cite

Abstract. The molecular machinery of deflagellation can be activated in detergent permeabilized Chlamydomonas reinhardtii by the addition of Ca 2+ (Sanders, M. A., and J. L. Salisbury, 1989. J. Cell Biol. 108:1751-1760). This suggests that stimuli which induce deflagellation in living cells cause an increase in the intracellular concentration of Ca 2+, but this has never been demonstrated. In this paper we report that the wasp venom peptide, mastoparan, and the permeant organic acid, benzoate, activate two different signalling pathways to trigger deflagellation. We have characterized each pathway with respect to: (a) the requirement for extracellular Ca2÷; (b) sensitivity to Ca 2+ channel blockers; and (c) 45Ca influx. We also report that a new mutant strain of C. reinhardtii, adf-1, is specifically defective in the acid-activated signalling pathway. Both signalling pathways appear normal in another mutant, fa-1, that is defective in the machinery of deflagellation (Lewin, R. and C. Burrascano. 1983. Experientia. 39:1397-1398Sanders, M. A., and J. L. Salisbury. 1989. J. Cell Biol. 108:1751-1760. We conclude that mastoparan induces the release of an intracellular pool of Ca 2+ whereas acid induces an influx of extraceUular Ca 2+ to activate the machinery of deflagellation.D FLAGELLATION is a specific event whereby the flagella are precisely excised from the cell body (Rosenbanm and Carlson, 1969;Satir et al., 1976;Lewin and Lee, 1985;Sanders and Salisbury, 1989; Jarvik and Suhan, 1991). The physical mechanism of flagellar excision appears to involve both a microtubule severing activity (Vale, 1991;Shiina et al., 1992;McNally and Vale, 1993) and a mechanical force generated by centrin (for references see Hartzell et al., 1993). A stellate array of centrin-containing transition zone fibers contract during deflagellation (Sanders and Salisbury, 1989). Chlamydomonas cells permeabilized with the non-ionic detergent, NP-40, deflagellate when Ca 2+ is added in /~M concentrations (Sanders and Salisbury, 1989). Because Ca 2÷ is necessary and sufficient for deflagellation in detergent-permeabilized cells (Sanders and Salisbury, 1994), agents which induce deflagellation in vivo may act via increases in intracellular [Ca2+]. Deflagellation can be produced in living cells by a variety of stimuli (Minz and Lewin, 1954;Thompson et al., 1974;Lewin et al., 1980;Witman, 1986). We have previously shown that acid flux into the cell triggers deflagellation in vivo (Hartzell et al., 1993) as does external application of the wasp venom peptide, mastoparan (Quarmby et al., 1992). We now pose the question: How do these agents generate an intracellular Ca 2÷ signal in vivo?Address all correspondence to L, M, Quarmby, Department of Anatomy and Cell Biology, Emory University School of Medicine, Atlanta, GA 30322.In the only published report to examine the requirement for extracellular Ca 2+ during acid-induced deflagellation, the authors state that a 30-min pretreatment in [Ca 2+] below 0.1 #M inhibited acid-induced deflagellation, but t...

show abstract

“…It has been suggested that in the absence of calcium, high concentrations of cadmium binds to adenosine triphosphate and does not affect smooth muscle phosphorylation [42].…”

Section: Discussionmentioning

confidence: 99%

Cadmium Reduces Contractile Responses of Rat Duodenum, In Vitro

Koç

Koçak

Akçıl

2008

Biol Trace Elem Res

View full text Add to dashboard Cite

The present study focuses on the effects of cadmium in drinking water on rat duodenum contractility, in vitro. Two experimental groups (n = 10 each) were administered with 15 ppm cadmium chloride in their drinking water for 1 and 2 months, respectively. Two separate groups (n = 10 each) were maintained in similar conditions but received no cadmium and acted as controls. After the experimental period, the duodenal segment responses were measured by means of an isotonic transducer. The average peak amplitude of acetylcholine-induced contractions was significantly decreased in both cadmium-treated groups. Incubation of duodena from the cadmium-free controls with atropine or in a calcium-free medium resulted in reduced contractility that was undistinguishable from that of the cadmium-treated rats. Cadmium reduces the contractile response apparently by directly or indirectly decreasing cellular calcium influx.

show abstract

Diverse actions of cadmium on the smooth muscle myosin phosphorylation system

Cited by 22 publications

References 17 publications

Placental Endocrine Disruption Induced by Cadmium: Effects on P450 Cholesterol Side-Chain Cleavage and 3β-Hydroxysteroid Dehydrogenase Enzymes in Cultured Human Trophoblasts

Placental Endocrine Disruption Induced by Cadmium: Effects on P450 Cholesterol Side-Chain Cleavage and 3β-Hydroxysteroid Dehydrogenase Enzymes in Cultured Human Trophoblasts

Two distinct, calcium-mediated, signal transduction pathways can trigger deflagellation in Chlamydomonas reinhardtii

Cadmium Reduces Contractile Responses of Rat Duodenum, In Vitro

Contact Info

Product

Resources

About