Cell culture, oxidative stress, and antioxidants: Avoiding pitfalls

Halliwell, Barry

doi:10.4103/2319-4170.128725

Cited by 150 publications

(185 citation statements)

References 82 publications

(122 reference statements)

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“…유전공학적인 방법은 bcl-2와 bcl-xL과 같은 anti-apoptotic 유전자의 과발현을 유도하여 세포 사멸을 억제한다 [8,9]. 또한, 배양조건의 조절을 통한 방법은 fed-batch나 perfusion 같은 공정을 변화시키거나 anti-apoptotic agent 첨가 또는 활 성 산소종 (Reactive oxygen species, ROS)의 억제 물질을 배 양 과정 중 첨가하여 세포 사멸을 억제할 수 있다 [10,11]. (Fig.…”

Section: Introductionunclassified

Effects of Storage-protein 2 Derived from Silkworm Hemolymph on Reduction of Aggregation and Cell Death in CHO Cells

임진혁¹,

차현명²,

김지훈³

et al. 2016

KSBB Journal

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Chinese hamster ovary (CHO) cells have been widely used for production of various recombinant proteins such as cytokines and monoclonal antibodies. The cell aggregation and cell death in CHO cell culture directly affect cell viability, and productivity and quality of products. In this study, we investigated preventing effects of storage-protein 2 (SP2) derived from silkworm hemolymph on cell aggregation and cell death in CHO cell culture producing albuminerythropoietin (Alb-EPO). The viable cell density in the culture supplemented with 2 mg/mL SP2 was 1.71-fold higher than that in control culture. Increased titer of Alb-EPO was also found in the culture with SP2. Morphology of CHO cells in SP2 supplemented cultures did not differ from that of control. In addition, the cell aggregation rate of the SP2 cultures was reduced 20% compared to the control. Finally, we confirmed that the apoptosis was strongly suppressed by addition of SP2 in the cultures. These results clearly demonstrate that SP2 can be served as an effective supplement for enhancing titer of Alb-EPO via reducing cell aggregation and cell death.

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Section: Introductionunclassified

Effects of Storage-protein 2 Derived from Silkworm Hemolymph on Reduction of Aggregation and Cell Death in CHO Cells

임진혁¹,

차현명²,

김지훈³

et al. 2016

KSBB Journal

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“…Cytotoxicity can be caused by several factors, including oxidative stress. Changes in the expression of antioxidant enzymes and in the synthesis or degradation of cellular thiols, increases in lipid peroxidation and protein oxidation are good markers of cellular oxidation [11,12]. On the other hand, disruption of thiol synthesis or oxidation of cellular thiols, particularly high oxidation of glutathione (GSH), may also be an underlying factor for cellular toxicity [11,12].…”

Section: Volume 1 Issue 5 -2015mentioning

confidence: 99%

Cellular and Molecular Aspects of Drug-Induced Liver Toxicity: Recent Prominent Mechanisms

Erkekoğlu¹

2015

MOJT

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Despite recent advances in drug development technologies, some drugs continue to be withdrawn from the market because of their late hepatotoxic effects. Drugs can cause liver toxicity through several molecular mechanisms, most of which need to be clarified by further research. Newly found drug-induced liver injury (DILI)-mechanisms like endoplasmic reticulum stress should also be considered while evaluating drug toxicity. New drugs launched in the market should be tested particularly for hepatotoxicity by using hepatic cell cultures and animal models continuously. Future research should target patients in the post-marketing phase in order to provide more evidence grounds to the clinical safety of potential drugs of high propensity of DILI. This review aims to draw the attention to the issue of cellular and molecular aspects of liver toxicity induced by drugs and address DILI as a potential clinical problem that needs further investigation.

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“…Although variable for different cell types, the typical growth parameters in cell culture are 37°C temperature, 5% CO 2 , and 95% humidity. Cell culture has been successfully used to evaluate safety, therapeutic efficacy and mechanisms of action of natural and synthetic compounds for their biological use (1). Cytotoxicity is the determinate potential of any compound or agent to kill cells.…”

Section: Introductionmentioning

confidence: 99%