Organophosphorus Compound-Induced Apoptosis in SH-SY5Y Human Neuroblastoma Cells

Carlson, Kent; Jortner, Bernard S.; Ehrich, Marion

doi:10.1006/taap.2000.8997

Cited by 100 publications

(61 citation statements)

References 78 publications

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“…However, apoptosis has been shown to be triggered by several factors, including exposure to pesticide. [33][34][35][36] Our results showed that cypermethrin produced cell injury and apoptosis in rat hepatocytes. Also cypermethrin-induced apoptosis in the telencephalon of tadpoles has been reported by Izaguirre et al (2000).…”

Section: )mentioning

confidence: 99%

The Pyrethroid Cypermethrin-Induced Biochemical and Histological Alterations in Rat Liver

Yavaşoğlu

Sayim

Uyanıkgil

et al. 2006

JOURNAL OF HEALTH SCIENCE

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Cypermethrin, a synthetic pyrethroid, has broadspectrum use in agriculture, domestic and veterinary applications due to its high bioefficacy, enhanced stability and considerably low mammalian toxicity. The objective of this study was to investigate the cypermetrin-induced alterations in the liver tissue of Wistar male rats, based on the histopatological, enzymological analyses and apoptotic changes. The animals of the experimental groups were orally fed with laboratory chow combined 60, 150, and 300 mg/kg Kral 250 EC during 28 consecutive days. At the end of the treatment, no significant change was found in relative liver weights, liver total proteins and cholinesterase enzyme activities of cypermethrin treated rats, when compared with control animals. Histopathological changes such as vacuolar degeneration, enlargement of the sinusoids, degeneration in hepatic cords and hepatocytes, vacuole formations in hepatocytes, pleomorphism in nucleus, and congestion were observed in liver tissues of only 150 and 300 mg/kg cypermethrin treated rats. Mononuclear cell infiltration and an increase in the Kupffer cells in liver parenchymatous tissue were also determined. In all cypermethrin treated groups, the apoptotic index in livers of rats was significantly increased compared to control group (p < 0.001). These results suggest that cypermethrin might cause hazardous effects in different levels to non-target organisms.

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Section: )mentioning

confidence: 99%

The Pyrethroid Cypermethrin-Induced Biochemical and Histological Alterations in Rat Liver

Yavaşoğlu

Sayim

Uyanıkgil

et al. 2006

JOURNAL OF HEALTH SCIENCE

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“…The dose of phosphamidon that we have selected in this study is based on earlier reports that phosphamidon like other organophosphates induces apoptosis/necrosis at concentrations ranging from 0 to 100 μM in SH-SY5Y human neuroblastoma cells [12]. Cells were also incubated with either 20 μM NAC or 25 μM curcumin to evaluate the attenuation effects.…”

Section: Isolation and Treatment Of Human Peripheral Blood Mononucleamentioning

confidence: 99%

Assessment of phosphamidon‐induced apoptosis in human peripheral blood mononuclear cells: Protective effects of N‐acetylcysteine and curcumin

Ahmed

Tripathi

Ahmed

et al. 2010

J Biochem & Molecular Tox

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The molecular mechanism for noncholinergic toxicity of phosphamidon, an extensively used organophosphate pesticide, is still not clear. The aim of the present study is to find the possible molecular mechanism of this pesticide to induce apoptosis and the role of different drugs for attenuation of such effects. Human peripheral blood mononuclear cells (PBMC) were incubated with increasing concentrations of phosphamidon (0-20 μM) for 6-24 h. The MTT assay reveals that phosphamidon induces cytotoxicity in a dose-dependent manner. Cellular glutathione (GSH) is depleted in a dose-dependent manner from 55% to 70% at concentrations between 10 and 20 μM. The percentage of cells that bind to Annexin-V, which is a representative of cells either undergoing apoptosis or necrosis during 24 h incubation, increases in a dose-dependent manner. Above 5 μM, significant necrosis of cells was observed. DNA fragmentation assay revealed that at low concentration of phosphamidon (1 μM), no appreciable change in DNA fragmentation was seen; however, distinct fragmentation was observed beyond 2.5 μM. Phosphamidon was found to cause significant depletion of GSH, which correlates well with the percentage of cells undergoing apoptosis. An increasing trend in levels of cytochrome c was observed with increasing concentration of phosphamidon, indicating that the apoptotic effect of phosphamidon is mediated through cytochrome c release. Coadministration of the antioxidants N-acetylcysteine and curcumin attenuated phosphamidon-induced apoptosis. This further supports our hypothesis that oxidative stress, as indicated by GSH depletion, results in the induction of apoptosis by release of cytochrome c.

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“…Loss of function of these transcription factors can lead to abnormal induction of genes related to generalized toxic stress responses, innate immunity, detoxication and response to ingested material [104]. OP exposure can also lead to apoptotic events in both mammals and C. elegans [133][134][135] and numerous genes and proteins involved in apoptosis have been shown to have altered expression levels. For instance, an anti-apoptotic gene found in humans (map-2) was down-regulated and the abundance of a protein involved in the engulfment stage of apoptosis (NEX-1) increased [32].…”

Section: Changes In Gene and Protein Expressionmentioning

confidence: 99%

Caenorhabditis elegans: An Emerging Model System for Pesticide Neurotoxicity

McVey

Mink²,

Snapp³

et al. 2012

J Environ Anal Toxicol

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Organophosphorus Compound-Induced Apoptosis in SH-SY5Y Human Neuroblastoma Cells

Cited by 100 publications

References 78 publications

The Pyrethroid Cypermethrin-Induced Biochemical and Histological Alterations in Rat Liver

The Pyrethroid Cypermethrin-Induced Biochemical and Histological Alterations in Rat Liver

Assessment of phosphamidon‐induced apoptosis in human peripheral blood mononuclear cells: Protective effects of N‐acetylcysteine and curcumin

Caenorhabditis elegans: An Emerging Model System for Pesticide Neurotoxicity

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