Measurement of doxorubicin-induced lipid peroxidation under the conditions that determine cytotoxicity in cultured tumor cells

Benchekroun, Mohamed Nabil; Robert, Jacques

doi:10.1016/0003-2697(92)90346-9

Cited by 21 publications

(7 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…24 In addition, adriamycin has been shown to induce production of ROS such as superoxide, hydrogen peroxide and hydroxyl radicals, which can modulate important cellular events including direct membrane effects, 41,42 lipid peroxidation 43,44 and mitochondrial function. 24 Hence, the antioxidant properties of flavonoids have been suggested to play a role in protection against adriamycin-induced toxicity.…”

Section: Discussionmentioning

confidence: 99%

The protective effects of melanoidins in adriamycin‐induced oxidative stress in isolated rat hepatocytes

et al. 2004

View full text Add to dashboard Cite

The importance of the antioxidants contained in foods is well recognized both for preserving the foods themselves and for supplying essential antioxidants in vivo. Among these, the melanoidins formed during food processing and storage represent a significant part of our diet, with an average intake of several grams per day. Melanoidins exhibit antioxidant properties in vitro through their protective effect against reactive oxygen species. Here we investigated the protective effect of the model glucose-glycine melanoidins on oxidative stress induced by adriamycin in hepatocytes isolated from rats. The study was performed by examining cell toxicity (lactate dehydrogenase) release in the medium, lipoperoxidation, protein oxidation, GSH and ATP levels. The addition of 50 µg glucose-glycine melanoidins to the hepatocytes treated with 25 and 75 µM of adriamycin decreased the cell oxidative damage. The cell toxicity, lipoperoxidation and the protein oxidation decreased significantly in the presence of melanoidins. The effect of melanoidins on the intracellular antioxidant GSH when co-incubated the adriamycin-hepatocytes with melanoidins resulted in a recovery of GSH levels. Furthermore, from the study of ATP levels we found that the damage to the mitochondria induced by adriamycin is decreased in the presence of melanoidins. According to these results, we suggest that melanoidins are capable of preventing cell oxidation. Based on these mechanisms, the ingestion of melanoidins present in food could be play a role important in the prevention of oxidative damage and prevention the diseases related to free radicals.

show abstract

Section: Discussionmentioning

confidence: 99%

The protective effects of melanoidins in adriamycin‐induced oxidative stress in isolated rat hepatocytes

et al. 2004

View full text Add to dashboard Cite

show abstract

“…In an attempt to show if this enhancement has a role to play in detoxifying the peroxides formed from the redox cycling of doxorubicin, we have developed a technique for the evaluation of these peroxides in cultured cells exposed to the drug [25]. We show in this paper that malondialdehyde, the end product of doxorubicin-induced lipid peroxidation, can be found in cell lines exhibiting low glutathione peroxidase activity, and that the enhancement of the activity, through constitutive or induced overexpression of the enzymes, is accompanied by an absence of doxorubicininduced formation of malondialdehyde in the cells.…”

mentioning

confidence: 99%

Doxorubicin‐induced lipid peroxidation and glutathione peroxidase activity in tumor cell lines selected for resistance to doxorubicin

Benchekroun

Pourquier

Schott

et al. 1993

European Journal of Biochemistry

Self Cite

View full text Add to dashboard Cite

Doxorubicin‐induced lipid peroxidation was evaluated in four human or murine cell strains in culture and in their doxorubicin‐resistant variants, by the quantification of malondialdehyde produced after a 2‐h incubation of cells with the drug. Significantly increased malondialdehyde levels were obtained 24 h after doxorubicin treatment in three of the wild‐type cell lines with doses as low as 0.05–0.1 μg/ml, which is within an order of magnitude of the concentration of the drug which inhibits cell growth by 50%. This production of malondialdehyde was abolished in two doxorubicinresistant strains, even with high doses of drug (100–300 μg/ml), but was maintained in the third resistant line. No malondialdehyde production was observed in the fourth cell line, sensitive or resistant. It is remarkable that an enhancement of selenium‐dependent and non‐selenium‐dependent glutathione peroxidase activities was exhibited during the acquisition of resistance to doxorubicin in the two first lines, but not in the third, whereas a constitutively high non‐selenium‐dependent glutathione peroxidase activity existed in the doxorubicin‐sensitive and doxorubicin‐resistant variants of the fourth cell line. Gene expression of selenium‐dependent glutathione peroxidase and of glutathione S‐transferase π, which is known partially to bear a non‐selenium‐dependent glutathione peroxidase activity, were correlated with the corresponding enzyme activities. It appears, therefore, that the already known enhancement of glutathione peroxidase activity and expression in doxorubicin‐resistant cell lines has a quantifiable consequence upon doxorubicin‐induced lipid peroxidation and may have consequences in the mechanism of resistance to this drug.

show abstract

“…We have already shown that there is a significant inverse relationship between glutathione peroxidase activity and doxorubicin-induced lipid peroxidation in cell lines of different origin [6]. We show here that the decrease in doxorubicin-induced lipid peroxidation observed in the resistant cells can also be attributed to a diminished formation of hydroxyl radical, which might be explained at least in part by an overactivity of superoxide dismutase in the resistant cells.…”

Section: May 1993 Febs Lettersmentioning

confidence: 50%

“…It appears from our work that the early development of doxorubicin resistance is not accompanied by a reduction of free radical production; the C6 0.001 and the C6 1V lines appear as pure MDR lines, their resistance to doxorubicin being only due to the overexpression of P-glycoprotein. In contrast, the C6 0.5 line, which can tolerate high intracellular amounts of drug, presents several features not directly associated with classical MDR: it is able to strongly decrease free radical formation, as shown in this paper; it is also able to avoid the doxorubicin-induced lipid peroxidation as shown earlier [6]. The C6 0.1 and C6 Rev lines behave somewhat like the C6 0.5 line, but the inhibition of DMPO adduct formation occurs to a much lesser extent.…”

Section: Discussionmentioning

confidence: 76%

“…This could be for instance the case of cells resistant to doxorubicin [3] especially since they have been shown to develop no DNA breaks at cytotoxic exposures [4]. We have recently shown that it was possible to evaluate the degree of doxorubicin-induced lipid peroxidation in tumor cells [5], and that it was related to the glutathione peroxidase activity of the cells [6]. We wanted then to know if this was related to the formation of oxygen free radicals; we have therefore evaluated the formation of hydroxyl radical upon doxorubicin exposure in cells sensitive and resistant to this drug, especially in cells having developed mechanisms of resistance other than P-glycoprotein overexpression, and displaying an intracellular tolerance to the drug [7].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Doxorubicin‐induced oxygen free radical formation in sensitive and doxorubicin‐resistant variants of rat glioblastoma cell lines

1993

Self Cite

View full text Add to dashboard Cite

We have studied the formation of hydroxyl radical (OH•) induced by doxorubicin in a series of doxorubicin‐ or vincristine‐selected variants of C6 rat glioblastoma cells in culture by electron‐spin resonance spectroscopy using 5,5′‐dimethyl‐1‐pyrroline‐1‐oxide as a spin trap. Wild‐type cells, sensitive to doxorubicin, exhibited in the presence of this drug a concentration‐dependent OH• formation which could be inhibited by preincubation with superoxide dismutase, catalase or an antibody against cytochrome P450‐reductase. In highly doxorubicin‐resistant cells, OH• formation was reduced to about 20% of the level obtained in sensitive cells. In cells presenting a very low level of resistance to doxorubicin or in cells selected with vincristine, both presenting a pure multidrug‐resistant phenotype, OH• formation was identical to that obtained in sensitive cells. In cells of intermediate resistance or in revertant cells, intermediate levels of OH• formation were obtained. Protection against OH• formation and action can be identified at the levels of superoxide dismutase and glutathione peroxidase activities, which are both enhanced in the resistant cells.

show abstract

Measurement of doxorubicin-induced lipid peroxidation under the conditions that determine cytotoxicity in cultured tumor cells

Cited by 21 publications

References 19 publications

The protective effects of melanoidins in adriamycin‐induced oxidative stress in isolated rat hepatocytes

The protective effects of melanoidins in adriamycin‐induced oxidative stress in isolated rat hepatocytes

Doxorubicin‐induced lipid peroxidation and glutathione peroxidase activity in tumor cell lines selected for resistance to doxorubicin

Doxorubicin‐induced oxygen free radical formation in sensitive and doxorubicin‐resistant variants of rat glioblastoma cell lines

Contact Info

Product

Resources

About