Toxicity and neuropharmacology of cyclopiazonic acid

Nishie, K.; Cole, Richard; Dorner, Joe W.

doi:10.1016/0278-6915(85)90284-4

Cited by 58 publications

(21 citation statements)

References 30 publications

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“…Inhibition of these ATPases by CPA results in cell death as a result of stress response and activation of apoptotic pathways (Venkatesh andVairamuthu 2005, Vinokurova et al 2007). In mice, CPA has an LD 50 of approximately 13 mg/kg (Nishie et al 1985) making consumption of a lethal dose unlikely, especially as there is no evidence that CPA accumulates in animal tissue. However, side effects of low doses have not been ruled out as its pharmacological properties are similar to classical antipsychotic drugs like reserpine and chlorpromazine (Nishie et al 1985).…”

Section: Cyclopiazonic Acidmentioning

confidence: 98%

“…In mice, CPA has an LD 50 of approximately 13 mg/kg (Nishie et al 1985) making consumption of a lethal dose unlikely, especially as there is no evidence that CPA accumulates in animal tissue. However, side effects of low doses have not been ruled out as its pharmacological properties are similar to classical antipsychotic drugs like reserpine and chlorpromazine (Nishie et al 1985). These side effects include hyperkinesias, hypothermia, Parkinson-like tremors, catalepsy, and convulsions.…”

Section: Cyclopiazonic Acidmentioning

confidence: 98%

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Functional Genomics to Improve Meat Quality in Pigs

Davoli¹,

Zambonelli²,

Braglia³

2012

OMICs Technologies

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Section: Cyclopiazonic Acidmentioning

confidence: 98%

Section: Cyclopiazonic Acidmentioning

confidence: 98%

Functional Genomics to Improve Meat Quality in Pigs

Davoli¹,

Zambonelli²,

Braglia³

2012

OMICs Technologies

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“…Tissue samples were obtained from a CL1-0 xenograft model, which was used to confirm the inhibitory effect of citreoviridin on tumor growth in vivo (20). Immunodeficient mice carrying subcutaneous CL1-0 tumors were abdominally injected with citreoviridin or DMSO and then sacrificed when control tumors reached a size of 1000 mm 3 . Proteins from the dissected tissues were digested and processed for phosphopeptide enrichment.…”

Section: Quantitative Analysis Of Dynamic Phosphorylation Profiles Ofmentioning

confidence: 99%

“…Citreoviridin is the pathogenic factor for several diseases, including acute cardiac beriberi (3) and Keshan disease (4). Many studies have elucidated the underlying mechanism of citreoviridin cytotoxicity in different cell types.…”

mentioning

confidence: 99%

Temporal Phosphoproteome Dynamics Induced by an ATP Synthase Inhibitor Citreoviridin*

Hsu

Wang³

et al. 2015

Molecular & Cellular Proteomics

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Citreoviridin, one of toxic mycotoxins derived from fungal species, can suppress lung cancer cell growth by inhibiting the activity of ectopic ATP synthase, but has limited effect on normal cells. However, the mechanism of citreoviridin triggering dynamic molecular responses in cancer cells remains unclear. Here, we performed temporal phosphoproteomics to elucidate the dynamic changes after citreoviridin treatment in cells and xenograft model. We identified a total of 829 phosphoproteins and demonstrated that citreoviridin treatment affects protein folding, cell cycle, and cytoskeleton function. Furthermore, response network constructed by mathematical modeling shows the relationship between the phosphorylated heat shock protein 90 β and mitogen-activated protein kinase signaling pathway. This work describes that citreoviridin suppresses cancer cell growth and mitogenactivated protein kinase/extracellular signal-regulated kinase signaling by site-specific dephosphorylation of HSP90AB1 on Serine 255 and provides perspectives in cancer therapeutic strategies. Molecular & Cellular

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“…TG, a naturally occurring sequiterpene lactone, is a nonphorbol ester type tum or promotor [8], It induces a rapid elevation of [Ca2+]j without generation of inositol phosphates in certain cell types. It has been shown that TG is a very potent inhibitor of ER Ca2+-ATPases, less effective on cardiac sarcoplasmic reticulum (SR) Ca2+-ATPase, and apparently ineffective against the enzyme from skeletal SR and plasma membrane [9], CPA is an indole tetramic acid metabolite of Aspergillus and Pénicillium [10]. It specifically inhibits ER/SR-Ca2+-ATPase and has no effects on N a+,K+-ATPase, H +,K+-ATPase, mitochondrial Fo/ Fi-ATPase, and plasma membrane (PM) Ca2+-ATPase [11].…”

Section: Introductionmentioning

confidence: 99%

Differential Effects of Endoplasmic Reticulum Ca<sup>2+</sup>-ATPase Inhibitors on Madin-Darby Canine Kidney Cells

Lien

Wang²,

Martı́nez-Zaguilán³

1995

Cell Physiol Biochem

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Endoplasmic reticulum (ER) Ca²⁺-ATPases regulate intracellular free calcium ([Ca²⁺]ⁱⁿ) in renal epithelial cells. Interestingly, treatment of certain cell types with ER Ca²⁺-ATPase inhibitors such as thapsigargin (TG), cyclopiazonic acid (CPA), and 2,5-di-tert-butyl-l,4-benzohydroquinone (BHQ) may result in distinct effects on [Ca²⁺]^m homeostasis. In this study, we investigated whether these distinct effects are due to Ca²⁺ entry after Ca²⁺ depletion of the ER. Therefore, we coloaded Madin-Darby canine kidney cells with SNARF-1 and Fura-2 (see text) to simultaneously measure intracellular pH (pHⁱⁿ) and [Ca²⁺]ⁱⁿ, respectively. Subsequently, Madin-Darby canine kidney cells were treated both in the presence and absence of extracellular Ca²⁺ ([Ca²⁺]^ex) with ER-Ca²⁺-ATPase inhibitors (TG, CPA, and BHQ). In the presence of [Ca²⁺]^ex, both TG and BHQ caused a sustained increase in [Ca²⁺]ⁱⁿ and a decrease in pH^ιn. In contrast, CPA induced a transient increase in [Ca²⁺]^m in the presence of [Ca²⁺]^ex. Acute [Ca²⁺]^ex removal resulted in a decrease in [Ca²⁺]ⁱⁿ. In the absence of [Ca²⁺]^ex, the [Ca²⁺]ⁱⁿ increase induced by either TG, CPA, or BHQ was suppressed. These data suggest that the TG-, BHQ-, and CPA-sensitive-Ca²⁺ pool is readily depleted by removal of [Ca²⁺]^ex. Readdition of [Ca²⁺]^ex increased [Ca²⁺]^ιn transiently in the absence of drugs. In the presence of CPA, the readdition of [Ca²⁺]^ex increased [Ca²⁺]ⁱⁿ also transiently. In contrast, readdition of [Ca²⁺]^ex resulted in a sustained increase in [Ca²⁺]ⁱⁿ when either TG or BHQ was present. This latter effect was reversed by subsequent addition of CPA (in the presence of [Ca²⁺]^ex), or when CPA was added prior to the readdition of [Ca²⁺]^ex. These data suggest that CPA, unlike TG and BHQ, also decreases Ca²⁺ entry across the plasma membrane. Altogether, our data indicate that ER Ca²⁺-ATPase inhibitors exhibit differential effects on [Ca²⁺]ⁱⁿ homeostasis in Madin-Darby canine kidney cells.

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Toxicity and neuropharmacology of cyclopiazonic acid

Cited by 58 publications

References 30 publications

Functional Genomics to Improve Meat Quality in Pigs

Functional Genomics to Improve Meat Quality in Pigs

Temporal Phosphoproteome Dynamics Induced by an ATP Synthase Inhibitor Citreoviridin*

Differential Effects of Endoplasmic Reticulum Ca<sup>2+</sup>-ATPase Inhibitors on Madin-Darby Canine Kidney Cells

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