ArticleOxidative medicine and cellular longevity2013
Oxidative stress and mitogen-activated protein kinase pathways involved in cadmium-induced BRL 3A cell apoptosis.
Article in Oxidative medicine and cellular longevity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18 citing papers in PubMed, 58 citations in OpenAlex.
- Multienzyme active melanin nanodots for antioxidant-immunomodulatory therapy of hyperoxia lung injury.Materials today. Bio · 2025Article
- Association of blood cadmium with all-cause and cause-specific mortality in patients with hypertension.Frontiers in public health · 2023Article
- ERK: A Double-Edged Sword in Cancer. ERK-Dependent Apoptosis as a Potential Therapeutic Strategy for Cancer.Cells · 2021Review
- Impact of Peels Extracts from an Italian Ancient Tomato Variety Grown under Drought Stress Conditions on Vascular Related Dysfunction.Molecules (Basel, Switzerland) · 2021Article
- Lead (Pb) Accumulation in Human THP-1 Monocytes/Macrophages In Vitro and the Influence on Cell Apoptosis.Biological trace element research · 2021Article
- Zinc Regulates Glucose Metabolism of the Spinal Cord and Neurons and Promotes Functional Recovery after Spinal Cord Injury through the AMPK Signaling Pathway.Oxidative medicine and cellular longevity · 2021Article
- Corilagin Ameliorates Con A-Induced Hepatic Injury by Restricting M1 Macrophage Polarization.Frontiers in immunology · 2021Article
- Article
- Inhibition of connexin 43 attenuates oxidative stress and apoptosis in human umbilical vein endothelial cells.BMC pulmonary medicine · 2020Article
- The Effect of Cadmium on Apoptotic Genes mRNA Expression of Bax and Bcl-2 in Small Intestine of Rats.Iranian journal of pathology · 2018Article
- Protective Role of UCP2 in Oxidative Stress and Apoptosis during the Silent Phase of an Experimental Model of Epilepsy Induced by Pilocarpine.Oxidative medicine and cellular longevity · 2018Article
- Gap junction blockage promotes cadmium-induced apoptosis in BRL 3A derived from Buffalo rat liver cells.Journal of veterinary science · 2016Article
- Role of autophagy in cadmium-induced apoptosis of primary rat osteoblasts.Scientific reports · 2016Article
- The Effects of Cadmium at Low Environmental Concentrations on THP-1 Macrophage Apoptosis.International journal of molecular sciences · 2015Article
- Salidroside Protects against Cadmium-Induced Hepatotoxicity in Rats via GJIC and MAPK Pathways.PloS one · 2015Article
- Cadmium induces apoptosis in primary rat osteoblasts through caspase and mitogen-activated protein kinase pathways.Journal of veterinary science · 2015Article
- Stress-induced stimulation of choline transport in cultured choroid plexus epithelium exposed to low concentrations of cadmium.American journal of physiology. Regulatory, integrative and comparative physiology · 2014Article
- Protective effect of calycosin-7-O-β-D-glucopyranoside against oxidative stress of BRL-3A cells induced by thioacetamide.Pharmacognosy magazineArticle
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, BRL 3A cells were treated with different Cd concentrations (0, 10, 20, and 40 μmol/L) for 12 h and preincubated with or without N-acetyl-L-cysteine (NAC) (2 mmol/L) for 30 min, and cells were treated with Cd (0 and 20 μmol/L), pretreated with p38 inhibitor (SB203580), JNK (c-Jun NH2-terminal kinases) inhibitor (SP600125), and extracellular signal-regulated kinase (ERK) inhibitor (U0126) for 30 min, and then treated with 20 μmol/L Cd for 12 h. Cd decreased cell viability, SOD, and GSH-Px activity in a concentration-dependent manner. Increased MDA level, ROS generation, nuclear condensation, shrinkage, and fragmentation in cell morphology were inhibited by NAC. Cd-induced apoptosis was attenuated by pretreatment with SB203580, SP600125, and U0126. The results of western blot showed that NAC preincubation affected Cd-activated MAPK pathways, p38 and ERK phosphorylation. Cd treatment elevated the mRNA levels of Bax and decreased the mRNA levels of Bcl-2, respectively. The same effect was found in their protein expression levels. These results suggest that oxidative stress and MAPK pathways participate in Cd-induced apoptosis and that the balance between pro- and antiapoptotic genes (Bax and Bcl-2) is important in Cd-induced apoptosis.
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