Induction of apoptotic erythrocyte death by rotenone

Lupescu, Adrian; Jilani, Kashif; Zbidah, Mohanad; Läng, Florian

doi:10.1016/j.tox.2012.06.007

Cited by 64 publications

(45 citation statements)

References 88 publications

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“…In addition, autoantibodies to DEK have been identified in juvenile rheumatoid arthritis, systemic lupus erythematosus and sarcoidosis. Previous studies have suggested that the DEK protein is closely associated with the apoptosis of cells, since it inhibits p53-mediated apoptosis, it works in combination with the viral oncogenes, E6 and E7, to overcome senescence in cells, and it also promotes Harvey Rat Sarcoma Viral Oncogene Homolog-driven keratinocyte transformation (4,(10)(11)(12). A study by Han et al (13) demonstrated that the DEK protein was closely associated with the proliferation of serous ovarian tumor cells, and that the overexpression of DEK was significantly associated with the increased proliferating index of Ki-67.…”

Section: Introductionmentioning

confidence: 99%

Overexpression of DEK is an indicator of poor prognosis in patients with gastric adenocarcinoma

Xia

Kong

et al. 2016

Oncology Letters

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Abstract. Increased expression of the human DEK proto-oncogene (DEK) gene has been associated with numerous human malignancies. The DEK protein is associated with chromatin reconstruction and gene transcription, and is important in cell apoptosis. The present study aimed to elucidate the role of DEK with regard to gastric adenocarcinoma tumor progression and patient prognosis. DEK protein expression was analyzed using immunohistochemistry in 192 tumors paired with adjacent non-cancerous gastric mucosa that had been surgically resected from patients with primary gastric adenocarcinoma. The association between DEK expression and the clinicopathological characteristics of the patients was evaluated using the χ 2 test and Fisher's exact test. The survival rates of the patients were calculated using the Kaplan-Meier method. Cox analysis evaluated the association between the expression of DEK and the survival rate of the patients. The DEK protein was expressed in 84 patients with gastric adenocarcinoma (43.8%) and in 20 of the paired normal gastric mucosa tissues (11.5%). The DEK expression rate was found to be associated with tumor size (P=0.006), tumor grade (P=0.023), lymph node metastasis (P=0.018), serous invasion (P=0.026), tumor stage (P=0.001) and Ki-67 expression (P=0.003). Furthermore, patients with gastric adenocarcinoma that expressed DEK had decreased disease-free (log-rank, 16.785; P<0.0001) and overall (log-rank, 15.759; P<0.0001) survival rates compared with patients without DEK expression. Patients with late-stage gastric adenocarcinoma that expressed DEK exhibited a lower overall survival rate compared with patients without DEK expression (P=0.002). Additional analysis revealed that DEK expression was an independent prognostic factor for the prognosis of gastric adenocarcinoma (hazard ratio, 0.556; 95% confidence interval, 0.337-0.918; P=0.022). From the results of the present study, it can be concluded that the detection of DEK protein expression in gastric adenocarcinoma tissues may be important for the diagnosis and prognosis of patients, and may be a targeted therapy for the treatment of gastric adenocarcinoma.

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Section: Introductionmentioning

confidence: 99%

Overexpression of DEK is an indicator of poor prognosis in patients with gastric adenocarcinoma

Xia

Kong

et al. 2016

Oncology Letters

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“…Accelerated suicidal erythrocyte death may contribute to the anemia of several clinical disorders and eryptosis may be triggered by a wide variety of xenobiotics [22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41,42,43,44,45]. …”

Section: Introductionmentioning

confidence: 99%

The Uremic Toxin Acrolein Promotes Suicidal Erythrocyte Death

Ahmed

Langer

Abed

et al. 2013

Kidney Blood Press Res

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Background: Anemia is a major complication of end stage renal disease. The anemia is mainly the result of impaired formation of erythrocytes due to lack of erythropoietin and iron deficiency. Compelling evidence, however, points to the contribution of accelerated erythrocyte death, which decreases the life span of circulating erythrocytes. Erythrocytes may enter suicidal death or eryptosis, which is characterized by cell shrinkage and by cell membrane scrambling with phosphatidylserine-exposure at the erythrocyte surface. Triggers of eryptosis include increase of cytosolic Ca²⁺-activity ([Ca²⁺]_i). Erythrocytes could be sensitized to cytosolic Ca²⁺ by ceramide. In end stage renal disease, eryptosis may possibly be stimulated by uremic toxins. The present study explored, whether the uremic toxin acrolein could trigger eryptosis. Methods: Cell volume was estimated from forward scatter, phosphatidylserine-exposure from annexin-V-binding, hemolysis from hemoglobin release, [Ca²⁺]_i from Fluo3-fluorescence, and ceramide from fluorescent antibodies. Results: A 48 h exposure to acrolein (30 － 50 µM) did not significantly modify [Ca²⁺]_i but significantly decreased forward scatter and increased annexin-V-binding. Acrolein further triggered slight, but significant hemolysis and increased ceramide formation in erythrocytes. Acrolein (50 µM) induced annexin-V-binding was significantly blunted in the nominal absence of extracellular Ca²⁺. Acrolein augmented the annexin-V-binding following treatment with Ca²⁺ ionophore ionomycin (1 µM). Conclusion: Acrolein stimulates suicidal erythrocyte death or eryptosis, an effect at least in part due to stimulation of ceramide formation with subsequent sensitisation of the erythrocytes to cytosolic Ca²⁺.

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“…Rotenone is toxic to erythrocytes in vitro [5]. Rotenoneinduced oxidative damage causes dopaminergic neuronal death [6] neuronal death occur in Parkinson's diseases [7].…”

Section: Introductionmentioning

confidence: 99%

Behavioral Studies of Wistar Rats in Rotenone Induced Model of Parkinson’s Disease

Priyanga

Krishnamurthy

Selvaraj

2017

Int J Pharm Pharm Sci

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Objective: The objective of the study was to determine the behavioral activities of Wistar rats induced with rotenone.Methods: Thirty-six male Wistar rats were taken for the study and divided into six groups of six rats each. Group-I is the vehicle-treated, Group-II animals were induced with rotenone (3 mg/kg/bwt) by i. p. Group-III were co-treated with rotenone and L-DOPA (10 mg/kg/bwt) orally, Group-IV were co-treated with rotenone and quercetin (25 mg/kg/bwt) orally, Group-V were co-treated with rotenone and hesperidin (50 mg/kg/bwt) orally, Group-VI were treated with rotenone, quercetin and hesperidin in the same dosage regime for 60 d. The behavioural tests, such as open field test, ladder climbing test and hanging wire test were performed. The biochemical parameters such as urea, creatinine and activities of ALT and AST were also analysed.Results: All data are expressed as the mean±SD. Disability was noted in the behaviour of rats induced with Parkinson's disease (PD). The deficits in behavioral activity were significantly changed when compared with an induced group (p<0.001) and biochemical parameters due to rotenone were significantly (p<0.001) restored by co-treatment with quercetin and hesperidin. Conclusion:In our in vivo study, we have demonstrated the combination of quercetin and hesperidin to serve as neuroprotective compounds by improving the behavioral abnormalities and restoring the biochemical parameters. Hence, these powerful antioxidants may protect brain cells.

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Induction of apoptotic erythrocyte death by rotenone

Cited by 64 publications

References 88 publications

Overexpression of DEK is an indicator of poor prognosis in patients with gastric adenocarcinoma

Overexpression of DEK is an indicator of poor prognosis in patients with gastric adenocarcinoma

The Uremic Toxin Acrolein Promotes Suicidal Erythrocyte Death

Behavioral Studies of Wistar Rats in Rotenone Induced Model of Parkinson’s Disease

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