Effects of H2O2 on the growth, secretion, and metabolism of hybridoma cells in culture

Ostrovidov, Serge; Franck, P.; Capiaumont, J.; Dousset, B.; Belleville, F.

doi:10.1007/s11626-998-0132-8

Cited by 16 publications

(8 citation statements)

References 27 publications

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“…Among ROS, H 2 O 2 is an important contributor to oxidative stress, which is converted from superoxide that leaks from mitochondria . H 2 O 2 addition significantly reduced cell growth and viability of mammalian cell lines by inducing ER‐mediated apoptosis . In this study, we also observed that H 2 O 2 addition in rCHO cell cultures increased the ROS level and ER stress, resulting in decreased cell growth and cell viability in a dose‐dependent manner.…”

Section: Discussionsupporting

confidence: 66%

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Baicalein Reduces Oxidative Stress in CHO Cell Cultures and Improves Recombinant Antibody Productivity

Hansen

Kol

et al. 2017

Biotechnology Journal

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Oxidative stress that naturally accumulates in the endoplasmic reticulum (ER) as a result of mitochondrial energy metabolism and protein synthesis can disturb the ER function. Because ER have a responsibility on the protein synthesis and quality control of the secreted proteins, ER homeostasis has to be well maintained. When H O , an oxidative stress inducer, is added to recombinant Chinese hamster ovary (rCHO) cell cultures, it reduced cell growth, monoclonal antibody (mAb) production, and galactosylated form of mAb in a dose-dependent manner. To find an effective antioxidant for rCHO cell cultures, six antioxidants (hydroxyanisole, N-acetylcysteine, baicalein, berberine chloride, kaempferol, and apigenin) with various concentrations are examined individually as chemical additives to rCHO cell cultures producing mAb. Among these antioxidants, baicalein shows the best mAb production performance. Addition of baicalein significantly reduced the expression level of BiP and CHOP along with reduced reactive oxygen species level, suggesting oxidative stress accumulated in the cells can be relieved using baicalein. As a result, addition of baicalein in batch cultures resulted in 1.7-1.8-fold increase in the maximum mAb concentration (MMC), while maintaining the galactosylation of mAb. Likewise, addition of baicalein in fed-batch culture resulted in 1.6-fold increase in the MMC while maintaining the galactosylation of mAb. Taken together, the results obtained here demonstrate that baicalein is an effective antioxidant to increase mAb production in rCHO cells.

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Section: Discussionsupporting

confidence: 66%

“…Previously, the negative effect of oxidative stress induced by H 2 O 2 addition on cell growth and viability was observed in mammalian cell lines such as hybridoma, HEK293, HeLa cells, and CHO cells . Among ROS, H 2 O 2 is an important contributor to oxidative stress, which is converted from superoxide that leaks from mitochondria .…”

Section: Discussionmentioning

confidence: 99%

Baicalein Reduces Oxidative Stress in CHO Cell Cultures and Improves Recombinant Antibody Productivity

Hansen

Kol

et al. 2017

Biotechnology Journal

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“…Individual species of oxygen-free radicalts are difficult to resolve with fluorescent indicators. For example, DHR is sensitive to superoxide but also to other ROS such as hydrogen peroxide and peroxynitirite (Rothe et al, 1991;Royall and Ischiropoulos, 1993;Bueb et al, 1995;Gilad et al, 1997;Ostrovidov et al, 1998;Gow et al, 1999). Thus, we turned to pharmacological approaches to further examine the contribution of ROS to the enhanced vulnerability of sublethally stretched neurons to NDMAR-mediated toxicity.…”

Section: Sublethal Stretch Produces High Levels Of Nonlethal Rosmentioning

confidence: 99%

“…In brief, DHR is oxidized to a fluorescent rhodamine-123 (Royall and Ischiropoulos, 1993), and the consequent rise in fluorescence may be used as an indicator of ROS production. DHR has been shown to be oxidized by superoxide anions (Rothe et al, 1991;Bueb et al, 1995;Ostrovidov et al, 1998), hydrogen peroxide (Royall and Ischiropoulos, 1993;Gow et al, 1999), peroxide radicals (Royall and Ischiropoulos, 1993;Gow et al, 1999), and peroxynitrite (Gilad et al, 1997). ROS were measured as described previously Aarts et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Vulnerability of Central Neurons to Secondary Insults afterIn VitroMechanical Stretch

Arundine¹,

Aarts²,

Lau³

et al. 2004

J. Neurosci.

118

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Mild traumatic brain injuries are of major public health significance. Neurons in such injuries often survive the primary mechanical deformation only to succumb to subsequent insults. To study mechanisms of vulnerability of injured neurons to secondary insults, we used an in vitro model of sublethal mechanical stretch. Stretch enhanced the vulnerability of the neurons to excitotoxic insults, causing nuclear irregularities, DNA fragmentation, and death suggestive of apoptosis. However, the DNA degradation was not attributable to classical (caspase mediated) or caspase-independent apoptosis. Rather, it was associated with profound stretch-induced mitochondrial dysfunction and the overproduction of reactive oxygen species (ROS). Sublethally stretched neurons produced surprisingly high levels of ROS, but these in isolation were insufficient to kill the cells. To be lethal, the ROS also needed to combine with nitric oxide (NO) to form the highly reactive species peroxynitrite. Peroxynitrite was not produced after stretch alone and arose only after combining stretch with an insult capable of stimulating NO production, such as NMDA or an NO donor. This explained the exquisite sensitivity of sublethally stretched neurons to a secondary NMDA insult. ROS scavengers and NO synthase (NOS) inhibitors prevented cell death and DNA degradation. Moreover, inhibiting neuronal NOS activation by NMDA using peptides that perturb NMDA receptor-postsynaptic density-95 interactions also reduced protein nitration and cell death, indicating that the reactive nitrogen species produced were neuronal in origin. Our data explain the mechanism of enhanced vulnerability of sublethally injured neurons to secondary excitotoxic insults and highlight the importance of secondary mechanisms to the ultimate outcome of neurons in mild neurotrauma.

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“…However, the weak neuroprotective effect of the potent hydroxyl radical scavenger melatonin (30) questions a remarkable contribution of hydroxyl radicals in our model. Growing evidence points to a sensitivity of DHR to oxidation by superoxide anions (31)(32)(33), which play an important role in NMDA receptor-mediated neurotoxicity (13,14). Increased superoxide anion generation by 3-OH-GA is indirectly supported by a potentiating effect of high concentrations of NO donor SNAP on 3-OH-GA toxicity, which is suggestive of peroxynitrite formation (17).…”

mentioning

confidence: 99%

Contribution of Reactive Oxygen Species to 3-Hydroxyglutarate Neurotoxicity in Primary Neuronal Cultures from Chick Embryo Telencephalons

et al. 2001

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Glutaryl-CoA dehydrogenase deficiency is an autosomal recessively inherited neurometabolic disorder with a distinct neuropathology characterized by acute encephalopathic crises during a vulnerable period of brain development. 3-Hydroxyglutarate (3-OH-GA), which accumulates in affected patients, has been identified as an endogenous neurotoxin mediating excitotoxicity via N-methyl-D-aspartate receptors. As increased generation of reactive oxygen species (ROS) and nitric oxide (NO) plays an important role in excitotoxic neuronal damage, we investigated whether ROS and NO contribute to 3-OH-GA neurotoxicity. 3-OH-GA increased mitochondrial ROS generation in primary neuronal cultures from chick embryo telencephalons, which could be prevented by MK-801, confirming the central role of N-methyl-D-aspartate receptor stimulation in 3-OH-GA toxicity. ROS increase was reduced by alpha-tocopherol and--less effectively-by melatonin. alpha-Tocopherol revealed a wider time frame for neuroprotection than melatonin. Creatine also reduced neuronal damage and ROS formation but only if it was administered >or=6 h before 3-OH-GA. NO production revealed only a slight increase after 3-OH-GA incubation. NO synthase inhibitor N(omega)-nitro-L-arginine prevented NO increase but did not protect neurons against 3-OH-GA. The NO donor S-nitroso-N-acetylpenicillamine revealed no effect on 3-OH-GA toxicity at low concentrations (0.5-5 microM), whereas it potentiated neuronal damage at high concentrations (50-500 microM), suggesting that weak endogenous NO production elicited by 3-OH-GA did not affect neuronal viability. We conclude from our results that ROS generation contributes to 3-OH-GA neurotoxicity in vitro and that radical scavenging and stabilization of brain energy metabolism by creatine are hopeful new strategies in glutaryl-CoA dehydrogenase deficiency.

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Effects of H2O2 on the growth, secretion, and metabolism of hybridoma cells in culture

Cited by 16 publications

References 27 publications

Baicalein Reduces Oxidative Stress in CHO Cell Cultures and Improves Recombinant Antibody Productivity

Baicalein Reduces Oxidative Stress in CHO Cell Cultures and Improves Recombinant Antibody Productivity

Vulnerability of Central Neurons to Secondary Insults afterIn VitroMechanical Stretch

Contribution of Reactive Oxygen Species to 3-Hydroxyglutarate Neurotoxicity in Primary Neuronal Cultures from Chick Embryo Telencephalons

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