The effect of acute and chronic exposure to acetaldehyde—a mutagenic metabolite of dietary ethanol—on prostate cancer cells: A potential source of race disparity disfavoring black men.

2012 ◽  
Vol 30 (5_suppl) ◽  
pp. 143-143
Author(s):  
Lionel Lloyds Banez ◽  
Anthony Kyle Davidson ◽  
Wiguins Etienne ◽  
Emma H Allott ◽  
Elizabeth Ellen Calloway ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Chronic Exposure ◽  
Acute Exposure ◽  
Exposure Model ◽  
Environment Interaction ◽  
Tumor Proliferation ◽  
Inhibition Of Proliferation ◽  
Tumor Doubling Time ◽  
Acute And Chronic Exposure

143 Background: We recently reported that the ADH1B*3 allele, which is specific to African Americans (AA), when combined with ethanol intake may constitute a gene-environment interaction leading to elevated prostate cancer (CaP) and potentially aggressive CaP risk among AA men possibly through intra-prostatic acetaldehyde accumulation. Indeed, studies have shown microsomes from rat ventral prostates biotransform ethanol to acetaldehyde that further metabolizes into oxidative stress-inducing acetyl radicals. In addition, acetaldehyde has been previously shown to enhance proliferation of colon cancer cells. Whether acetaldehyde has the same effect on CaP is unknown. Methods: We subjected DU-145 CaP cells to varying concentrations of acetaldehyde using acute and chronic models of exposure and measured tumor proliferation using MTS assay. Proliferation was measured over 4 days of acetaldehyde treatment in acute and after 2 weeks of treatment in chronic exposure experiments. All experiments were conducted in triplicate. Results were expressed as mean values for each treatment referenced to untreated cells. Doubling times were calculated using least squares fitting exponential regression. Results: In the acute exposure model, proliferation of DU-145 cells was inhibited by 150 uM acetaldehyde by 28% while 1,500uM and higher concentrations resulted in complete inhibition of proliferation. After chronic exposure to acetaldehyde, proliferation of DU-145 cells was inhibited by 500 uM acetaldehyde by 19%. In contrast, chronic exposure with 1,000 uM acetaldehyde resulted in increased proliferation by 9% and shortened tumor doubling time. Conclusions: Acute exposure to acetaldehyde resulted in inhibition of CaP cellular proliferation. Chronic exposure to high acetaldehyde concentrations promoted tumor proliferation likely through selection for more robust CaP cells that survive the repeated chemical insult. Our results suggest that chronic acetaldehyde exposure of existent CaP may potentially promote disease aggressiveness. Uncovering mechanisms for enhanced CaP cell proliferation by acetaldehyde are warranted.

scholarly journals Prostate Cancer: Treatments and Diagnosis

Bionatura ◽  
2019 ◽  
Vol 02 (Bionatura Conference Serie) ◽  
Author(s):  
Robert Angulo ◽  
Bryan Herrera ◽  
Keila Ibarra
Keyword(s):  
Prostate Cancer ◽  
Clinical Trials ◽  
Cancer Cells ◽  
Advanced Cancer ◽  
The Body ◽  
Tumor Proliferation ◽  
Cancer Treatments ◽  
Prostate Tumors ◽  
Prostate Cancer Treatments

Prostate cancer is a disease in which malignant (cancer) cells form in the tissues of the prostate. Prostate tumors were responsible for nearly six thousand deaths in Spain in 2016 as the symptoms are very silent and appear like advanced cancer or when this cancer has proliferated to other organs and senses. Therefore, there are 4 characteristic stages of this type of cancer that are classified according to their extension in the body. To make the diagnosis of this type of disease there are methods that in many cases show to be effective and in others not depending on the stage in which you are. Therefore, the number of treatments against prostate cancer has been increasing over the years from medications that help prevent tumor proliferation to strong surgeries. These treatments are not a solution to fight cancer, they simply have the function of maintaining cancer and its proliferation in order to generate a suitable lifestyle for patients for a time. Currently, several investigations have focused on combating prostate cancer through clinical trials that promise to generate favorable and acceptable solutions for patients.

Effects of sorafenib on proliferation of hormone-sensitive and hormone-insensitive prostate cancer cells

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. e16092-e16092
Author(s):  
Z. Culig ◽  
S. Jung Oh ◽  
F. R. Santer ◽  
M. Puhr ◽  
H. Steiner ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cell Number ◽  
Cyclin Dependent Kinase ◽  
Prostate Cancer Cells ◽  
Inhibition Of Proliferation ◽  
Sorafenib Treatment ◽  
Cellular Models

e16092 Background: Sorafenib is a multi-targeted kinase inhibitor approved for treatment of renal and hepatocellular cancer. In patients with castration therapy-resistant prostate cancer sorafenib treatment is associated with discordant prostate-specific antigen (PSA) and clinical responses, possibly due to an effect on PSA expression. The mechanisms of its action in advanced prostate tumors are not investigated so far. The aim of the present study was to evaluate the effects of sorafenib in androgen-sensitive (LNCaP) and -insensitive (PC 3) prostate cancer cell lines. Methods: Proliferation was evaluated by measurement of cell number and protein. Expression of cell cycle and apoptosis regulatory proteins of the Bcl-2 family was determined by Western blot. Results: Treatment of those cells by sorafenib for 48 hours resulted in a concentration-dependent inhibition of proliferation. Maximal inhibition was achieved with 25 μM of the compound. Cell number was reduced by 50% in both cell lines. We observed inhibition of expression of cyclin-dependent kinase 2 in LNCaP and PC3 cells. In addition, Mcl-1 protein, that is frequently overexpressed in prostate cancer, was down-regulated by sorafenib in both cellular models. Conclusions: Sorafenib caused inhibition of growth of prostate cancer cells regardless of their androgen sensitivity. Its inhibitory effects on cyclin- dependent kinase 2 and Mcl-1 imply that sorafenib regulates cell cycle progression and apoptosis in prostate cancer. On the basis of these results experiments with chemotherapy-resistant prostate cells are being performed. [Table: see text]

scholarly journals Analysis of Transcriptome, Selected Intracellular Signaling Pathways, Proliferation and Apoptosis of LNCaP Cells Exposed to High Leptin Concentrations

2019 ◽  
Vol 20 (21) ◽  
pp. 5412 ◽  
Author(s):  
Marta Szyszka ◽  
Lukasz Paschke ◽  
Marianna Tyczewska ◽  
Karol Jopek ◽  
Piotr Celichowski ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Intracellular Signaling ◽  
Gene Set Enrichment Analysis ◽  
Mitogen Activated Protein Kinase ◽  
Lncap Cells ◽  
Prostate Cancer Cells ◽  
Inhibition Of Proliferation ◽  
Proliferation And Apoptosis

Leptin, the first discovered adipokine, has been connected to various physiological and pathophysiological processes, including cancerogenesis. Increasing evidence confirms its influence on prostate cancer cells. However, studies on the effects of leptin on the proliferation and apoptosis of the androgen-sensitive LNCaP line of prostate cancer cells brought conflicting results. Therefore, we performed studies on the effects of high LEP concentration (1 × 10−6 M) on gene expression profile, change of selected signaling pathways, proliferation and apoptosis of LNCaP cells. RTCA (real-time cell analyzer) revealed inhibitory effect of LEP on cell proliferation, but lower LEP concentrations (10−8 and 10−10 M) did not affect cell division. Moreover, flow cytometry with a specific antibody for Cleaved PARP-1, an apoptosis marker, confirmed the activation of apoptosis in leptin-exposed LNCaP line of prostate cancer cells. Within 24 h LEP (10−6 M) increases expression of 297 genes and decreases expression of 119 genes. Differentially expressed genes (DEGs) were subjected to functional annotation and clusterization using the DAVID bioinformatics tools. Most ontological groups are associated with proliferation and apoptosis (seven groups), immune response (six) and extracellular matrix (two). These results were confirmed by the Gene Set Enrichment Analysis (GSEA). The leptin’s effect on apoptosis stimulation was also confirmed using Pathview library. These results were also confirmed by qPCR method. The results of Western Blot analysis (exposure to LEP 10 min, 1, 2, 4 and 24 h) suggest (after 24 h) decrease of p38 MAPK, p44-42 mitogen-activated protein kinase and Bcl-2 phosphorylated at threonine 56. Moreover, exposure of LNCaP cells to LEP significantly stimulates the secretion of matrix metallopeptidase 7 (MMP7). Obtained results suggest activation of apoptotic processes in LNCaP cells cultured at high LEP concentration. At the same time, this activation is accompanied by inhibition of proliferation of the tested cells.

scholarly journals Effect of garlic extract on mortality and biochemical parameters of fresh water fishes Heteropneustes fossilis against Cypermethrin

2019 ◽  
Vol 9 (2) ◽  
pp. 14-19
Author(s):  
Akanksha Singh ◽  
Kaneez Zahra
Keyword(s):  
Chronic Exposure ◽  
Biochemical Parameters ◽  
Chronic Toxicity ◽  
Garlic Extract ◽  
Acute Exposure ◽  
Exposure Level ◽  
Heteropneustes Fossilis ◽  
Blood Samples ◽  
Acute And Chronic Exposure ◽  
Remarkable Reduction

To find out the effect of garlic extract (GE) on mortality different concentrations of GE (1ml/l, 2ml/l, 5ml/l & 10ml/l) were administered along with the LC50 values of cypermethrin after 24, 48, 72 & 96 h exposures and 10 ml/l of GE was found to be effective at which no mortality occurred. To analyze the effect of GE on biochemical parameters after acute exposure of cypermethrin, fishes were divided into 4 groups of 10 fishes each. Ist group served as control, IInd, IIIrd and IVth group were treated with toxicant (24h LC50), GE (10ml/l) and toxicant + GE respectively. Same protocol was employed using 48-96 h LC50 values & 10ml/l GE. For chronic toxicity experiments fishes were divided into 4 groups of 10 fishes each. Ist group taken as control, IInd group contained 1/10th of 96 h LC50 of CYP, IIIrd group contained 10ml/l GE and in IVth group GE (10ml/l) + CYP (1/10th of 96 h LC50) for 15 days. Experiments were also carried out after 30 and 45 days exposure by same protocol. After acute and chronic exposure periods blood samples were collected, centrifuged and serum was separated to analyze biochemical parameters. Increased level of SGOT, SGPT, ALP, ACP, Creatinine, and Blood Glucose were observed during both acute and chronic exposure. Activity of Total protein was found to be decreased following acute and chronic exposure. Level of Uric acid increased in acute exposure but decreased during chronic exposure. However, garlic extract supplementation showed a remarkable reduction to these changes and all the parameters tends to become normalize. Our data indicate that garlic is a powerful antioxidant against cypermethrin induced toxicity. Keywords: Cypermethrin, Garlic extract, Heteropneustus fossilis, LC50.

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