HepG2 In Vitro TBARS Assay (Oxidative Stress)

CAT#: ITS-1022-YF1215
Target Cell Organism: Human
Target Cell Alternative Name: Hep G2
Target Cell Name: HepG2
Assay Type: Oxidative Stress Assays
Assay Overview
This assay is to provide HepG2-based In Vitro TBARS Assay (Oxidative Stress) to accelerate our client's oncology projects. The assay will be customized according to the specific requirements. Please contact our scientists to discuss more details.
Target Cell Name
HepG2
Target Cell Organism
Human
Target Cell Background
Hep G2 is an immortal cell line which was derived in 1975 from the liver tissue of a 15-year-old Caucasian male from Argentina with a well-differentiated hepatocellular carcinoma. These cells are epithelial in morphology, have a modal chromosome number of 55, and are not tumorigenic in nude mice.
Target Cell Alternative Name
Hep G2
Related Diseases
Hepatocellular Carcinoma
Research Area
Oncology
Assay Name
In Vitro TBARS Assay (Oxidative Stress)
Short Description
HepG2-cell based In Vitro TBARS Assay (Oxidative Stress)
Assay Description
The thiobarbituric acid reactive substances (TBARS) assay is one of the most common assays used to evaluate lipid peroxidation. In this assay, thiobarbituric acid reacts with malondialdehyde, which is one of the end products of lipid peroxidation (oxidative stress). Lipid peroxidation in cancer cells, plasma, urine and tissue can be assayed using the TBARS assay.
Assay Alternative Names
Thiobarbituric Acid Reactive Substances Assay
Assay Type
Oxidative Stress Assays
Assay Type Details
Disturbance between the production of reactive oxygen species (ROS), free radicals and antioxidant mechanisms is defined as the oxidative stress, or more precisely, it is an imbalance between the oxidant and antioxidant state in cells. This imbalance can cause harmful effects to cells and biomolecules, which ultimately causes adverse effects in the whole organism. Oxidative imbalance can target important proteinsand lipids in cells, which can increase the risk of developing a cancer. On the other hand, increased ROS production in cancer cells by certain cancer drugs can also arrest cancer cell cycle and cause senescence and apoptosis through oxidative stress.
For Research Use Only | Not For Clinical Use
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