Selenium protects the hypoxia induced apoptosis in neuroblastoma cells through upregulation of Bcl-2

Sarada, S.K.S; Patir, Himadri; Ruma, D.; Sharma, Shivani; Pauline, T; Mrinalini, _

doi:10.1016/j.brainres.2008.02.041

Cited by 48 publications

(44 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This is in agreement with previous studies that showed that the administration of nicotine results in a significant depletion of glutathione content in the cells [28]. Studies have shown that glutathione content increased significantly in selenium-treated hypoxic cells [29]. We have also observed a significant increase in the concentration of glutathione in selenium-treated cells compared to the control group.…”

Section: Discussionsupporting

confidence: 93%

Effects of Exogenous Selenium on Nicotine-Induced Oxidative Stress in Rats

Sreekala

Indira

2009

Biol Trace Elem Res

View full text Add to dashboard Cite

The effect of two different doses of selenium [1 and 50 microg selenium/100 g body weight (wt)] on nicotine-induced oxidative damage in liver was investigated in experimental rats. Male albino rats were maintained for 60 days as follows: (1) control group (normal diet), (2) nicotine group (0.6 mg/kg body wt)/day, (3) high-dose selenium (50 microg/100 g body wt)/day, (4) high-dose selenium (50 microg/100 g body wt) + nicotine (0.6 mg/kg body wt)/day, (5) low-dose selenium (1 microg/100 g body wt)/day, and (6) low-dose selenium (1 microg/100 g body wt) + nicotine (0.6 mg/kg body wt)/day. Nicotine administration caused a decrease in the activity of antioxidant enzymes, an increase in the concentration of lipid peroxidation products and protein carbonyls and an increase in the activity of nitric oxide synthase compared to the control group. Coadministration of nicotine and selenium reduced the concentration of lipid peroxidation products and increased the activity of antioxidant enzymes compared to the nicotine group. Selenium also enhanced the metabolism of nicotine. The antioxidant effect was more significant in the group administered a low dose of selenium.

show abstract

Section: Discussionsupporting

confidence: 93%

Effects of Exogenous Selenium on Nicotine-Induced Oxidative Stress in Rats

Sreekala

Indira

2009

Biol Trace Elem Res

View full text Add to dashboard Cite

show abstract

“…DEN has been built up as an intense hepatocarcinogen in rats that conceivably inspires its belongings through adjustments of DNA structure, particularly, by means of the arrangement of alkyl DNA adducts and the acceptance of reduction of Bcl-2/Bax ratios (Ma et al 2008). CASP-3 initiation assumes a focal part in the execution of apoptosis and is a typical occasion in two noteworthy pathways: the internal and external cell death pathways (Sarada et al 2008). In the current experiment, DEN exposure hindered the statement of CASP-3, while LBC and FnC 60 actuated the outflow of CASP-3.…”

Section: Discussionmentioning

confidence: 99%

Role and potential targeting of hepatic apurinic/apyrimidinic endonuclease-1 and cyclin-dependent kinase-4 in hepatocellular carcinoma

2018

Can. J. Physiol. Pharmacol.

View full text Add to dashboard Cite

“…NF-B fine-tunes Prdx6 expression at normal physiological conditions, while overactivation of NF-B during oxidative stress represses Prdx6 transcription in cell background (13,27). NF-B acts in both proapoptotic and apoptotic roles, depending on the cellular microenvironment (53,56). Prdx6-deficient cells display higher expression of ROS and overstimulation of NF-B, while Prdx6 optimizes the activity of NF-B, suggesting that loss of Prdx6 during oxidative stress leads to NF-B-mediated suppression of Prdx6.…”

Section: Discussionmentioning

confidence: 99%