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Journal articles on the topic 'Doxorubicine – Toxicologie'

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Published: 9 September 2023

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1

V., Rakshitha B., Nalini G. K., Sahana G. N., Deepak P., Jayashree V. Nagaral, Mohith N., and Divyashree C. R. "Comparison of safety and toxicity of liposomal versus conventional Doxorubicin: an updated review." International Journal of Basic & Clinical Pharmacology 8, no. 6 (May 23, 2019): 1453. http://dx.doi.org/10.18203/2319-2003.ijbcp20192220.

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Cancer persists to be a major cause of hospitalization and death every year. With the passage of time, new formulations of anticancer drugs are being introduced to the market and are drawing the concern of healthcare professionals in terms of the superiority, toxicology, and cost-effectiveness of the new formulations in comparison to the conventional formulation of the same drugs. Doxorubicin, a highly potent chemotherapeutic agent, it comes with three formulations (pegylated liposomal, nonpegylated liposomal and non-liposomal conventional formulations). English-language literature of the three formulations of Doxorubicin has been reviewed to inform the healthcare professionals regarding the differences between these formulations. Liposomal Doxorubicin promotes better toxicology profile than non-liposomal conventional Doxorubicin with an increased cost. Due to very limited studies, the cost-effectiveness of liposomal Doxorubicin is not well defined. Apart from that, this review highlights the inter patient variability in regard to the clearance and volume of distribution following the administration of liposomal Doxorubicin. In conclusion, further studies regarding the superiority of liposomal formulation of Doxorubicin , efficacy and dose standardization of liposomal Doxorubicin should be sought in the near future in a more better way.

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Bressolle, Fran�oise, Jeanne-Marie Jacquet, Marc Galtier, Jacques Jourdan, Daniel Donadio, and Jean-Fran�ois Rossi. "Doxorubicin and doxorubicinol plasma concentrations and excretion in parotid saliva." Cancer Chemotherapy and Pharmacology 30, no. 3 (1992): 215–18. http://dx.doi.org/10.1007/bf00686315.

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3

Jacquet, Jeanne-Marie, Fran�oise Bressolle, Marc Galtier, Magali Bourrier, Daniel Donadio, Jacques Jourdan, and Jean-Fran�ois Rossi. "Doxorubicin and doxorubicinol: intra-and inter-individual variations of pharmacokinetic parameters." Cancer Chemotherapy and Pharmacology 27, no. 3 (1990): 219–25. http://dx.doi.org/10.1007/bf00685716.

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4

Cusack, Barry J., Stephan P. Young, Joni Driskell, and Richard D. Olson. "Doxorubicin and doxorubicinol pharmacokinetics and tissue concentrations following bolus injection and continuous infusion of doxorubicin in the rabbit." Cancer Chemotherapy and Pharmacology 32, no. 1 (1993): 53–58. http://dx.doi.org/10.1007/bf00685876.

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5

Tan, Jun, Jingfen Ye, Meijun Song, Mi Zhou, and Yaoren Hu. "Ribavirin augments doxorubicin's efficacy in human hepatocellular carcinoma through inhibiting doxorubicin-induced eIF4E activation." Journal of Biochemical and Molecular Toxicology 32, no. 1 (November 7, 2017): e22007. http://dx.doi.org/10.1002/jbt.22007.

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6

Duncan, R., J. K. Coatsworth, and S. Burtles. "Preclinical toxicology of a novel polymeric antitumour agent: HPMA copolymerdoxorubicin (PK1)." Human & Experimental Toxicology 17, no. 2 (February 1998): 93–104. http://dx.doi.org/10.1177/096032719801700204.

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N-(2-hydroxypropyl)methacrylamide (HPMA) copolymer-doxorubicin (PK1) is a novel polymeric anticancer agent containing doxorubicin (approximately 8 wt%) bound to the polymer backbone via a Gly-Phe-Leu-Gly peptidyl linker. The approximate LD50 of PK1 in MF1 mice after a single i.v. injection was 63 mg/kg (doxorubicin-equivalent). Single doses of PK1 were administered to MF1 mice at 22.5 or 45 mg/kg and blood samples taken on days 3, 7 and 14 for haematological examination and clinical chemistry. At day 14 all animals were sacrificed for necropsy. In a multiple dose study, PK1 was administered i.v. to MF1 mice or Wistar rats (20 animals per group) weekly for five consecutive weeks at doses of 12.0 or 22.5 mg/kg (mice) or 3 and 5 mg/kg (rats). After 31 days 10 animals from each group were sacrificed for necropsy and the remainder were sacrificed after 59 days. Blood samples were taken 3 days after administration of each dose and at the end of the experiment, and urine samples were collectedonthe day prior to sacrifice.Mortality inthe single dose mouse and multiple dose rat studies was low. In the multiple dose mouse study 4/10 animals were killed in extremis before the scheduled day 31 and all animals died before day 37. PK1 induced a reduction in WBC and platelets in rats and mice shortly after treatment and RBC at later times, and in the single dose study alanine and aspartate aminotransferase levels were elevated at higher doses. Liver damage was seen only in rat tissue during histological examination. Other histological changes induced by PK1 include thymic and testicular atrophy, bone marrow depletion gastrointestinal tract changes and in the multiple dose study an increase in nuclear size in the proximal tubules of the kidney (although no changes in urine were seen). Recovery from these effects was seen in rats at 59 days. A PK1 dose of 20 mg/m2 (doxorubicin equivalent) was recommended as a safe dose for the start of Phase I clinical trials.

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Dewi, Ermi Girsang, Ali Nafiah Nasution, and Liena. "The Effect of Salam Leaf Ethanol Extract on the Histopathology of Doxorubicin-Induced Rats and its Effectiveness in Protecting the Heart Compared with Positive Control (Vitamin E)." International Journal of Science and Environment (IJSE) 1, no. 1 (November 21, 2021): 8–14. http://dx.doi.org/10.51601/ijse.v1i1.2.

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This study aims to determine the effect of bay leaf ethanol extract on the histopathological picture of the kidneys of rats induced by doxorubicin. To determine the administration of bay leaf ethanol extract is more effective in protecting the heart than the positive control (Vitamin E). The bay leaves used were obtained from the Harjosari II Medan Amplas area of Medan city. The independent variable in this study was Salam Leaf Ethanol Extract, while the dependent variable was kidney histopathology. This research was conducted at the Pharmacology and Toxicology Laboratory of the Faculty of Pharmacy, University of North Sumatra. The results showed that the administration of vitamin E together with doxorubicin showed a better renal histopathological picture. Vitamin E as a basic antioxidant is able to reduce the damage caused by doxorubicin which is seen in the absence of widening in the Bowman capsule.

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8

Rodrigues, Daniela, Luke Coyle, Barbara Füzi, Sofia Ferreira, Heeseung Jo, Bram Herpers, Seung-Wook Chung, et al. "Unravelling Mechanisms of Doxorubicin-Induced Toxicity in 3D Human Intestinal Organoids." International Journal of Molecular Sciences 23, no. 3 (January 24, 2022): 1286. http://dx.doi.org/10.3390/ijms23031286.

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Doxorubicin is widely used in the treatment of different cancers, and its side effects can be severe in many tissues, including the intestines. Symptoms such as diarrhoea and abdominal pain caused by intestinal inflammation lead to the interruption of chemotherapy. Nevertheless, the molecular mechanisms associated with doxorubicin intestinal toxicity have been poorly explored. This study aims to investigate such mechanisms by exposing 3D small intestine and colon organoids to doxorubicin and to evaluate transcriptomic responses in relation to viability and apoptosis as physiological endpoints. The in vitro concentrations and dosing regimens of doxorubicin were selected based on physiologically based pharmacokinetic model simulations of treatment regimens recommended for cancer patients. Cytotoxicity and cell morphology were evaluated as well as gene expression and biological pathways affected by doxorubicin. In both types of organoids, cell cycle, the p53 signalling pathway, and oxidative stress were the most affected pathways. However, significant differences between colon and SI organoids were evident, particularly in essential metabolic pathways. Short time-series expression miner was used to further explore temporal changes in gene profiles, which identified distinct tissue responses. Finally, in silico proteomics revealed important proteins involved in doxorubicin metabolism and cellular processes that were in line with the transcriptomic responses, including cell cycle and senescence, transport of molecules, and mitochondria impairment. This study provides new insight into doxorubicin-induced effects on the gene expression levels in the intestines. Currently, we are exploring the potential use of these data in establishing quantitative systems toxicology models for the prediction of drug-induced gastrointestinal toxicity.

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9

Candussio, Luigi, Giuliana Decorti, Enrico Crivellato, Marilena Granzotto, Anna Rosati, Tullio Giraldi, and Fiora Bartoli. "Toxicologic and pharmacokinetic study of low doses of verapamil combined with doxorubicin." Life Sciences 71, no. 26 (November 2002): 3109–19. http://dx.doi.org/10.1016/s0024-3205(02)02175-6.

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10

Che, Feifei, Yu Liu, and Caigang Xu. "Prevention and Treatment of Doxorubicin-Induced Cardiotoxicity by Dexrazoxane and Schisandrin B in Rabbits." International Journal of Toxicology 30, no. 6 (October 12, 2011): 681–89. http://dx.doi.org/10.1177/1091581811415873.

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The cost of dexrazoxane, a drug used to provide protection from doxorubicin-induced cardiotoxicity, limits its use in low-income countries. We aimed to see whether schisandrin B, an inexpensive drug, could provide protection equivalent to that provided by dexrazoxane. New Zealand white rabbits were randomly divided into groups and treated with saline, doxorubicin, doxorubicin + dexrazoxane, or doxorubicin + schisandrin B. Doxorubicin-induced damage and the protective effects were studied by recording the echocardiographic parameters and serum levels of superoxide dismutase, malondialdehyde, cardiac troponin I, and brain natriuretic peptide and observing the histology and degree of apoptosis. Schisandrin B had dose-dependent effects in decreasing the magnitude of doxorubicin-induced indicators of cardiomyopathy to a degree that approximated the decrease produced by dexrazoxane treatment. Schisandrin B might be a useful, low-cost alternative drug for this application.

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11

Yurtcu, E., ÖD İşeri, and FI Sahin. "Genotoxic and cytotoxic effects of doxorubicin and silymarin on human hepatocellular carcinoma cells." Human & Experimental Toxicology 33, no. 12 (March 27, 2014): 1269–76. http://dx.doi.org/10.1177/0960327114529453.

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The aim of this study was to investigate genotoxic and cytotoxic effects of doxorubicin, silymarin, or in combination on HepG2 cells for 24 and 48 h. Both doxorubicin and silymarin caused dose-dependent inhibition of cell proliferation. After 48 h of treatment, doxorubicin application caused dramatically increased ratio of apoptotic cells. Both 24 and 48 h of silymarin and doxorubicin–silymarin combination caused significant increases in the rate of apoptotic cells. Applications of doxorubicin and silymarin separately for 24 h led to deoxyribonucleic acid (DNA) damages. After 48 h of incubation, doxorubicin-induced genotoxic damage was 2-fold higher than the silymarin-induced damage. After 24 and 48 h, DNA damage in response to combined applications of doxorubicin and silymarin was indifferent from silymarin- and doxorubicin-induced damage respectively. There was not any difference in genotoxicity levels between incubation periods in combined applications of doxorubicin and silymarin. Lipid peroxidation levels increased in all applications. Biopharmacotherapy with chemotherapeutic agents are of interest in the issue of adjuvant therapy. Here, we demonstrate in vitro potential genotoxic and cytotoxic antitumor effect of silymarin on HepG2 cells at achievable plasma level concentrations.

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12

Kratz, F., G. Ehling, H.-M. Kauffmann, and C. Unger. "Acute and repeat-dose toxicity studies of the (6-maleimidocaproyl)hydrazone derivative of doxorubicin (DOXO-EMCH), an albumin-binding prodrug of the anticancer agent doxorubicin." Human & Experimental Toxicology 26, no. 1 (January 2007): 19–35. http://dx.doi.org/10.1177/0960327107073825.

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The (6-maleimidocaproyl)hydrazone derivative of doxorubicin (DOXO-EMCH) is an albumin-binding prodrug of doxorubicin with acid-sensitive properties that demonstrates superior antitumor efficacy in murine tumor models, and has been evaluated in a phase I study. In order to establish the toxicity profile of this prodrug, acute and repeat-dose toxicity studies were performed with DOXO-EMCH in CD1-mice, Sprague-Dawley rats and Beagle dogs. Although the objective of the acute toxicity studies was not the determination of LD50 values, the LD50 of DOXO-EMCH was >60mg/kg doxorubicin equivalents in both male and female mice (the LD50 of doxorubicin in CD-1 mice is ~12 mg/kg). In Sprague-Dawley rats, the LD50 was 23.4 and 45.9 mg/kg doxorubicin equivalents for males and females, respectively. For comparison, the LD50 of doxorubicin in Sprague-Dawley rats is ~10.5 mg/kg. The major clinical sign noted following intravenous administration of DOXOEMCH in mice and rats was a dose-dependent peripheral neuropathy which, in general, developed as a delayed toxicity 1-3 weeks after application. The observed neurotoxicity has been well documented for Sprague-Dawley rats treated with doxorubicin at a dose of 5 and 10 mg/kg. In Beagle dogs, LD10 was not reached for DOXO-EMCH at 4.5 mg/kg doxorubicin equivalents. A four-cycle intravenous study with DOXO-EMCH at dose levels of 4×2.5, 5.0 or 7.5 mg/kg doxorubicin equivalents in rats revealed approximately three-fold less side effects on the hemolymphoreticular system when compared to 4×2.5 mg/kg doxorubicin dose, whereas effects on the testes/oligospermia seem to be comparable between both drugs at equitoxic dose. A No Observable Adverse Effect Level (NOAEL) for DOXO-EMCH of 4×2.5 mg/kg doxorubicin equivalents was established in this study. This dose is equivalent to the maximum tolerated dose (MTD) of doxorubicin in rats. In a two-cycle study over a period of 6 weeks in Beagle dogs (intravenous administration of DOXO-EMCH at dose levels of 1.5, 3.0 or 4.5 mg/kg doxorubicin equivalents), dose-related systemic histamine-like reactions within the first 3 hours after injection were noted in all treated groups. Only transient and temporary effects on hematology, urinary function, as well as on histopathology in mid- and/or high-dose animals, were observed. The low dose of 2×1.5 mg/kg was considered to be the NOAEL in this study, which is equivalent to twice the MTD of doxorubicin in Beagle dogs. In summary, the toxicity studies with DOXO-EMCH in mice, rats or dogs have not identified any other special toxicity when compared to the toxicity data for doxorubicin. Preclinical tolerance of DOXO-EMCH was higher in mice, rats and dogs compared to doxorubicin. A dose of 20 mg/m2 doxorubicin equivalents was recommended as the starting dose for a phase I study with DOXO-EMCH.

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13

Makwana, Vivek, A/Prof Shailendra-Anoopkumar Dukie, and Santosh Rudrawar. "Investigating the Impact of OGT Inhibition on Doxorubicin- and Docetaxel-Induced Cytotoxicity in PC-3 and WPMY-1 Cells." International Journal of Toxicology 39, no. 6 (August 27, 2020): 586–93. http://dx.doi.org/10.1177/1091581820948433.

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Reduction in sensitivity in terms of cytotoxicity is responsible for therapy failure in patients undergoing chemotherapy with first-line anticancer drug molecules. A plethora of literature evidence points out that increased O-linked β- N-acetylglucosamine transferase (OGT) enzyme level/hyper- O-GlcNAcylation has direct implications in development of cancer and interferes with clinical outcomes of chemotherapy via interaction with oncogenic factors. The aim of this research was to evaluate the combination approach of anticancer drugs with an OGT inhibitor (OSMI-1) as an alternative way to resolve issues in the treatment of prostate cancer and assess the benefits offered by this approach. Effect of combination of doxorubicin and docetaxel with OSMI-1 on drug-induced cell death and synergism/antagonism was investigated using resazurin assay. Reduction in OGT enzyme level was evaluated using ELISA kit. Caspase-3/7 fluorescence assay was performed to detect apoptosis induction in PC-3 cells after treatment with the combinations of doxorubicin and OGT inhibitor to further understand the mechanism of cell death by concomitant treatment. Studies reveal that combination approach is indeed effective in terms of reducing the half-maximum growth inhibition value of doxorubicin when concomitantly treated with OSMI-1 and has synergistic effect in prostate cancer cells. PC-3 cells exhibited elevated levels of OGT enzyme in comparison to WPMY-1, and OSMI-1 has potential to inhibit OGT enzyme significantly. Data show that OSMI-1 alone and in combination with doxorubicin reduces OGT enzyme level significantly accompanied by increased apoptosis in prostate cancer cells. Combination of doxorubicin with OSMI-1 reduced the elevated OGT level which led to a drastic increase in sensitivity of PC-3 cells toward doxorubicin in comparison to doxorubicin alone. This finding provides important insight regarding alternative treatment strategies for effective management of cancer.

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14

Duncan, R., J. K. Coatsworth, and S. Burtles. "Preclinical toxicology of a novel polymeric antitumour agent: HPMA copolymer-doxorubicin (PK1)." Human & Experimental Toxicology 17, no. 2 (February 1, 1998): 93–104. http://dx.doi.org/10.1191/096032798678908378.

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15

Poljaková, Jitka, Tomáš Eckschlager, Jana Hřebačková, Jan Hraběta, and Marie Stiborová. "The comparison of cytotoxicity of the anticancer drugs doxorubicin and ellipticine to human neuroblastoma cells." Interdisciplinary Toxicology 1, no. 2 (September 1, 2008): 186–89. http://dx.doi.org/10.2478/v10102-010-0036-9.

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The comparison of cytotoxicity of the anticancer drugs doxorubicin and ellipticine to human neuroblastoma cellsEllipticine is an antineoplastic agent, whose mode of action is based mainly on DNA intercalation, inhibition of topoisomerase II and formation of covalent DNA adducts mediated by cytochromes P450 and peroxidases. Here, the cytotoxicity of ellipticine to human neuroblastoma derived cell lines IMR-32 and UKF-NB-4 was investigated. Treatment of neuroblastoma cells with ellipticine was compared with that of these cancer cells with doxorubicin. The toxicity of ellipticine was essentially the same as that of doxorubicin to UKF-NB-4 cells, but doxorubicin is much more effective to inhibit the growth of the IMR-32 cell line than ellipticine. Hypoxic conditions used for the cell cultivation resulted in a decrease in ellipticine and/or doxorubicin toxicity to IMR-32 and UKF-NB-4 neuroblastoma cells.

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16

Wallace, Kendall B. "Doxorubicin-Induced Cardiac Mitochondrionopathy." Pharmacology & Toxicology 93, no. 3 (September 2003): 105–15. http://dx.doi.org/10.1034/j.1600-0773.2003.930301.x.

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Kunarajah, Kuhan, Stefanie Hennig, Ross L. G. Norris, Michael Lobb, Bruce G. Charles, Ross Pinkerton, and Andrew S. Moore. "Population pharmacokinetic modelling of doxorubicin and doxorubicinol in children with cancer: is there a relationship with cardiac troponin profiles?" Cancer Chemotherapy and Pharmacology 80, no. 1 (April 25, 2017): 15–25. http://dx.doi.org/10.1007/s00280-017-3309-6.

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Callies, Sophie, Dinesh P. de Alwis, James G. Wright, Alan Sandler, Michael Burgess, and Leon Aarons. "A population pharmacokinetic model for doxorubicin and doxorubicinol in the presence of a novel MDR modulator, zosuquidar trihydrochloride (LY335979)." Cancer Chemotherapy and Pharmacology 51, no. 2 (February 2003): 107–18. http://dx.doi.org/10.1007/s00280-002-0542-3.

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19

Llesuy, Susana F., and Silvia Lores Arnaiz. "Hepatotoxicity of mitoxantrone and doxorubicin." Toxicology 63, no. 2 (August 1990): 187–98. http://dx.doi.org/10.1016/0300-483x(90)90042-f.

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20

Combs, Alan B., and Daniel Acosta. "Toxic Mechanisms of the Heart: A Review*." Toxicologic Pathology 18, no. 4a (January 1990): 583–96. http://dx.doi.org/10.1177/019262339001804a08.

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Toxic injury is one of the many ways by which the functional integrity of the heart may become compromised. Any of the subcellular elements may be the target of toxic injury, including all of the various membranes and organelles. Understanding the mechanisms underlying cardiotoxicity may lead to treatment of the toxicity or to its prevention. Doxorubicin and its analogs are very important cancer chemotherapeutic agents that can cause cardiotoxicity. Other agents which are cardiotoxic and which have profound public health implications include the alkaloid emetine in ipecac syrup, cocaine, and ethyl alcohol. The most important cardiotoxic mechanisms proposed for doxorubicin include oxidative stress with its resultant damage to myocardial elements, changes in calcium homeostasis, decreased ability to produce ATP, and systemic release of cardiotoxic humoral mediators from tissue mast cells. Each of the first 3 mechanisms can lead to each of the other 2, and the causal relationships between all of these mechanisms are not clear. New evidence suggests that doxorubicinol, one of the metabolites of doxorubicin may be the moiety responsible for cardiotoxicity. Several other potential mechanisms also have been proposed for doxorubicin. Emetine in ipecac syrup is the first aid treatment of choice for many acute toxic oral ingestions and the alkaloid, itself, is used to treat amebiasis. Cardiotoxicity occurs following chronic exposure, such as occurs therapeutically in amebiasis and with ipecac abuse by bulemics. A number of mechanisms are proposed for emetine cardiotoxicity, but the current mechanistic literature is quite scarce. Cocaine abuse recently has caught the public interest, in particular because of the drug-related sudden deaths of certain athletes. Cocaine can cause hypertension, arrhythmias, and reduced coronary blood flow, each of which can contribute to its lethality. However, it may be possible that cocaine sudden death episodes are more related to hyperthermia and convulsive seizures, rather than to cardiovascular toxicity. Chronic alcohol use leads to dilated cardiomyopathy and failure as part of the general physical degeneration that occurs with alcoholism. Several mechanisms are proposed for the cardiomyopathy, but only 2 things seem clear. The cardiotoxicity is due to an intrinsic effect of alcohol, rather than to malnutrition or co-toxicity, and abstinence is the only effective treatment for the cardiomyopathy. Recent articles indicate that very moderate use of alcohol may be beneficial and protect against cardiovascular-related morbidity. One explanation for these findings seems to be that the non-drinking groups, against whom the moderate drinking comparisons were made, were enriched in former drinkers with significant alcohol-related cardiovascular pathology.

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Murugesan Sudha and Thangarasu Vetrichelvan. "Genoprotective effect of D-Pinitol isolated from aerial parts of Soybean plants against Doxorubicin-induced genotoxicity evaluated by in vitro comet assay in Vero cell lines." International Journal of Research in Pharmaceutical Sciences 12, no. 2 (May 5, 2021): 1379–84. http://dx.doi.org/10.26452/ijrps.v12i2.4694.

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Doxorubicin is a chemotherapeutic agent with a genotoxic effect on normal cells at its therapeutic dose itself. D-Pinitol is an abundantly available carbohydrate in Soybean plants and has been proven for antioxidant and anti-inflammatory activities. Our investigation was examined by in vitro comet assay to explore the genoprotective effect of D-Pinitol in normal cells against Doxorubicin-induced genotoxicity in Vero cell lines. In vitro comet assay treatment groups were: Vero Cell lines with culture medium (control group), Doxorubicin (0.15μg/ml), D-Pinitol (0.05×103 mM, 0.125×103 mM, and 0.25×103 mM) alone, and pretreatment with D-Pinitol (0.05×103 mM, 0.125×103 mM, and 0.25×103 mM) before Doxorubicin (0.15μg/ml) treatment. When compared to the control group, D-Pinitol alone treated groups showed no significant changes in the percentage of DNA damage. For the evaluation of the genoprotective effect of D-Pinitol, the % DNA damage in the D-Pinitol, and Doxorubicin simultaneously treated groups were compared to the Doxorubicin alone treated group. The results showed that Doxorubicin-induced genotoxic effect in Vero cell lines was significantly reduced by D-Pinitol in a dose-dependent manner by reducing DNA damage. Our findings confirmed that D-Pinitol had no genotoxic effect and it showed a genoprotective effect against Doxorubicin-induced genotoxicity.

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An, Jie, and M. Saeed Sheikh. "Toxicology of Trastuzumab: An Insight into Mechanisms of Cardiotoxicity." Current Cancer Drug Targets 19, no. 5 (April 24, 2019): 400–407. http://dx.doi.org/10.2174/1568009618666171129222159.

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Trastuzumab is a humanized monoclonal antibody that is approved for the treatment of breast and gastric malignancies. Although it has shown promise as a biotherapeutic, its cardiotoxicity remains a major concern. Genotoxic anticancer anthracyclines such as doxorubicin and epirubicin are also known for their cardiotoxic effects. However, trastuzumab and anthracyclines are suggested to mediate cardiotoxicity via different pathways. The available lines of evidence suggest that trastuzumab can exacerbate the cardiotoxic effects of anthracyclines and thus, prior exposure to anthracyclines is regarded as one of the risk factors for trastuzumab-induced cardiotoxcity. Although it is generally believed that the trastuzumab-induced cardiotoxic effects are reversible, various preclinical studies have revealed its apoptotic effects on cardiomyocytes. Thus, the issue of the reversibility of its cardiotoxic effects remains to be fully resolved. This article discusses various mechanisms that have been proposed for the cardiotoxic effects of trastuzumab and the potential risk factors that can lead to cardiotoxicity. The recently approved anti-HER2 monoclonal antibodies including pertuzumab and ado-trastuzumab (T-DM1) are also discussed.

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Santos, GC, MR Almeida, LMG Antunes, and MLP Bianchi. "Effect of bixin on DNA damage and cell death induced by doxorubicin in HL60 cell line." Human & Experimental Toxicology 35, no. 12 (July 11, 2016): 1319–27. http://dx.doi.org/10.1177/0960327116630352.

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Bixin is a natural red pigment extracted from annatto. Although it is widely used as a coloring agent in food, there are few studies about the effect of this carotenoid on DNA. This study aimed to investigate the effects of bixin on cytotoxicity and genotoxicity induced by doxorubicin in HL60 cells. At concentrations above 0.3 μg/mL, bixin demonstrated cytotoxic effects in HL60 cells. Furthermore, this carotenoid was neither mutagenic nor genotoxic to HL60 cells and reduced the DNA damage induced by doxorubicin. Bixin and doxorubicin showed no apoptotic effect in HL60 cells, but the simultaneous combined treatments showed an increase in the percentage of apoptotic cells. In conclusion, our results showed that bixin modulates the cytotoxicity of doxorubicin via induction of apoptosis. The results of this study provide more knowledge about the toxic effects of anticancer treatments and how the natural compounds can be useful on these therapeutic approaches.

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Hong, C. Y., B. N. Chiang, J. Ku, and P. Wu. "Screening the in vitro Sperm-immobilizing Effect of some Anticancer Drugs." Human Toxicology 4, no. 4 (July 1985): 461–64. http://dx.doi.org/10.1177/096032718500400412.

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1 The in vitro sperm-immobilizing effect of seven anticancer agents, namely cyclophosphamide, 5-fluorouracil, cytarabine, mitomycin-C, 6-mercaptopurine, doxorubicin and vinblastine were screened with a transmembrane migration method. 2 Only doxorubicin and vinblastine inhibited human sperm motility. 3 Because colchicine, a microtubular inhibitor, had no sperm-immobilizing effect, we suggest that the sperm membrane is the site of action of these two anticancer drugs to inhibit human sperm motility.

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Satyam, Shakta Mani, Laxminarayana Kurady Bairy, Prakashchandra Shetty, P. Sainath, Sanjay Bharati, Akheruz Zaman Ahmed, Varun Kumar Singh, and A. J. Ashwal. "Metformin and Dapagliflozin Attenuate Doxorubicin-Induced Acute Cardiotoxicity in Wistar Rats: An Electrocardiographic, Biochemical, and Histopathological Approach." Cardiovascular Toxicology 23, no. 2 (February 2023): 107–19. http://dx.doi.org/10.1007/s12012-023-09784-8.

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AbstractDoxorubicin is a widely used anticancer drug whose efficacy is limited due to its cardiotoxicity. There is no ideal cardioprotection available against doxorubicin-induced cardiotoxicity. This study aimed to investigate the anticipated cardioprotective potential of metformin and dapagliflozin against doxorubicin-induced acute cardiotoxicity in Wistar rats. At the beginning of the experiment, cardiac screening of experimental animals was done by recording an electrocardiogram (ECG) before allocating them into the groups. Thereafter, a total of thirty healthy adult Wistar rats (150–200 g) were randomly divided into five groups (n = 6) and treated for eight days as follows: group I (normal control), group II (doxorubicin control), group III (metformin 250 mg/kg/day), group IV (metformin 180 mg/kg/day), and group V (dapagliflozin 0.9 mg/kg/day). On the 7th day of the treatment phase, doxorubicin 20 mg/kg was administered intraperitoneal to groups II, III, IV, and V. On the 9th day (immediately after 48 h of doxorubicin administration), blood was collected from anesthetized animals for glucose, lipid profile, CK-MB & AST estimation, and ECG was recorded. Later, animals were sacrificed, and the heart was dissected for histopathological examination. We found that compared to normal control rats, CK-MB, AST, and glucose were significantly increased in doxorubicin control rats. There was a significant reversal of doxorubicin-induced hyperglycemia in the rats treated with metformin 250 mg/kg compared to doxorubicin control rats. Both metformin (180 mg/kg and 250 mg/kg) and dapagliflozin (0.9 mg/kg) significantly altered doxorubicin-induced ECG changes and reduced the levels of cardiac injury biomarkers CK-MB and AST compared to doxorubicin control rats. Metformin and dapagliflozin protected the cellular architecture of the myocardium from doxorubicin-induced myocardial injury. Current study revealed that both metformin and dapagliflozin at the FDA-recommended antidiabetic doses mitigated doxorubicin-induced acute cardiotoxicity in Wistar rats. The obtained data have opened the perspective to perform chronic studies and then to clinical studies to precisely consider metformin and dapagliflozin as potential chemoprotection in the combination of chemotherapy with doxorubicin to limit its cardiotoxicity, especially in patients with comorbid conditions like type II diabetes mellitus.

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Zhen, Juan, Haitao Yu, Honglei Ji, Lu Cai, Jiyan Leng, and Bradley B. Keller. "Neonatal murine engineered cardiac tissue toxicology model: Impact of dexrazoxane on doxorubicin induced injury." Life Sciences 239 (December 2019): 117070. http://dx.doi.org/10.1016/j.lfs.2019.117070.

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Mattila, Minttu, Mirva Söderström, Liisa Ailanen, Eriika Savontaus, and Mikko Savontaus. "The Effects of Neuropeptide Y Overexpression on the Mouse Model of Doxorubicin-Induced Cardiotoxicity." Cardiovascular Toxicology 20, no. 3 (December 6, 2019): 328–38. http://dx.doi.org/10.1007/s12012-019-09557-2.

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AbstractDoxorubicin is a potent anticancer drug with cardiotoxicity hampering its use. Neuropeptide Y (NPY) is the most abundant neuropeptide in the heart and a co-transmitter of the sympathetic nervous system that plays a role in cardiac diseases. The aim of this work was to study the impact of NPY on doxorubicin-induced cardiotoxicity. Transgenic mice overexpressing NPY in noradrenergic neurons (NPY-OEDβH) and wild-type mice were treated with a single dose of doxorubicin. Doxorubicin caused cardiotoxicity in both genotypes as demonstrated by decreased weight gain, tendency to reduced ejection fraction, and changes in the expression of several genes relevant to cardiac pathology. Doxorubicin resulted in a tendency to lower ejection fraction in NPY-OEDβH mice more than in wild-type mice. In addition, gain in the whole body lean mass gain was decreased only in NPY-OEDβH mice, suggesting a more severe impact of doxorubicin in this genotype. The effects of doxorubicin on genes expressed in the heart were similar between NPY-OEDβH and wild-type mice. The results demonstrate that doxorubicin at a relatively low dose caused significant cardiotoxicity. There were differences between NPY-OEDβH and wild-type mice in their responses to doxorubicin that suggest NPY to increase susceptibility to cardiotoxicity. This may point to the therapeutic implications as suggested for NPY system in other cardiovascular diseases.

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Simon, Deborah L. "Comment: Doxorubicin Extravasations." DICP 23, no. 11 (November 1989): 928. http://dx.doi.org/10.1177/106002808902301126.

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Hacker-Klom, Ursula B., Marvin L. Meistrich, and Wolfgang Göhde. "Effect of doxorubicin and 4′-epi-doxorubicin on mouse spermatogenesis." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 160, no. 1 (March 1986): 39–46. http://dx.doi.org/10.1016/s0027-5107(96)90007-x.

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H. Abdulrazzaq, Munaf. "Protective Effect of Benfotiamine against Doxorubicin-Induced Cardiotoxicity in Rabbits." Iraqi Journal of Pharmaceutical Sciences ( P-ISSN: 1683 - 3597 , E-ISSN : 2521 - 3512) 16, no. 1 (March 31, 2017): 14–17. http://dx.doi.org/10.31351/vol16iss1pp14-17.

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The protective effect of benfotiamine against doxorubicin-induced cardiotoxicity was evaluated in rabbits. Pretreatment of rabbits with 70mg/kg benfotiamine orally 7 days before induction of cardiotoxicity with I.V 15mg/kg doxorubicin. injection resulted in significant reduction of the activities of lactate dehydrogenase and creatine phosphokinase enzyme in the serum compared to doxorubicin treated animals; benfotiamine also improves the histological changes produced by doxorubicin in the cardiac muscle compared to control. In conclusion, benfotiamine when used concomitantly with doxorubicin protects the myocardium against the cardiotoxicity induced by this cytotoxic drug.

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Turdi, Subat, Peisheng Xu, Qun Li, Youqing Shen, Parhat Kerram, and Jun Ren. "Amidization of doxorubicin alleviates doxorubicin-induced contractile dysfunction and reduced survival in murine cardiomyocytes." Toxicology Letters 178, no. 3 (May 2008): 197–201. http://dx.doi.org/10.1016/j.toxlet.2008.03.010.

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Erdogmus Ozgen, Zeynep, Meral Erdinc, İlker Kelle, Levent Erdinc, and Yusuf Nergiz. "Protective effects of necrostatin-1 on doxorubicin-induced cardiotoxicity in rat heart." Human & Experimental Toxicology 41 (January 2022): 096032712110660. http://dx.doi.org/10.1177/09603271211066066.

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Background: Doxorubicin (Dox) is one of the most effective antineoplastic drugs which has severe cardiotoxic effects, limiting its clinical usage. Though the exact mechanism of doxorubicin-induced cardiotoxicity is yet to be elucidated, it is shown that production of reactive oxygen species (ROS) increases oxidative stress and leads to cardiomyocyte apoptosis and necroptosis which is also defined as a programmed cell death. Purpose: In the present study, we investigate the effects of necrostatin-1 (Nec-1)—an inhibitor of receptor interaction proteins 1 (RIP1) and necroptosis—on doxorubicin-induced cardiotoxicity in rats. Research Design: Hearts were isolated and perfused by the Langendorff system in all four groups. Perfusion pressure (PP), left ventricular developed pressure (LVDP) and heart rate per minute (HR), LV (dP/dt) max, and LV (dP/dt) min which shows cardiac contractility and relaxation were recorded. Results: Results showed that PP significantly increased with Dox treatment and significantly decreased with Nec-1 treatment, while HR, LVDP, LV (dP/dt) max, and LV (dP/dt) min values significantly decreased with the Dox-treated group and significantly increased with Nec-1 treatment. Also with Nec-1 treatment, gene expression levels of anti-apoptotic Bcl-2 significantly increased and pro-apoptotic protein Bax, apoptotic marker caspase-3, and Nox-2 significantly decreased compared to the Dox-treated group. In heart tissues, MDA levels were significantly increased with Dox and decreased with Nec-1 treatment. These results were supported by the histological analysis indicated that Nec-1 reduced doxorubicin-induced cellular injury. Conclusions: In conclusion, our data indicate that Nec-1 ameliorates doxorubicin-induced cardiotoxicity by reducing oxidative stress injury and attenuating apoptosis and necroptosis.

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Powell, S. "Inhibition of doxorubicin-induced membrane damage by thiol compounds: Toxicologic implications of a glutathione-dependent microsomal factor." Free Radical Biology and Medicine 18, no. 2 (February 1995): 159–68. http://dx.doi.org/10.1016/0891-5849(94)00109-w.

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Takahashi, Hikari, Hitoshi Tainaka, Masakazu Umezawa, Ken Takeda, Hiromitsu Tanaka, Yoshitake Nishimune, and Shigeru Oshio. "Evaluation of testicular toxicology of doxorubicin based on microarray analysis of testicular specific gene expression." Journal of Toxicological Sciences 36, no. 5 (2011): 559–67. http://dx.doi.org/10.2131/jts.36.559.

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Gołuński, Grzegorz, Agnieszka Borowik, Dariusz Wyrzykowski, Anna Woziwodzka, and Jacek Piosik. "Pentoxifylline as a modulator of anticancer drug doxorubicin. Part I: Reduction of doxorubicin DNA binding." Chemico-Biological Interactions 242 (December 2015): 291–98. http://dx.doi.org/10.1016/j.cbi.2015.10.008.

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Dantas, Danielle, Amanda Gomes Pereira, Anderson Seiji Soares Fujimori, Ana Paula Dantas Ribeiro, Carol Cristina Vágula de Almeida Silva, Marina Gaiato Monte, Camila Renata Corrêa, et al. "Doxycycline Attenuates Doxorubicin-Induced Cardiotoxicity by Improving Myocardial Energy Metabolism in Rats." Journal of Cardiovascular Development and Disease 9, no. 8 (August 8, 2022): 254. http://dx.doi.org/10.3390/jcdd9080254.

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Aim: Evaluate the influence of doxycycline, an anti-inflammatory and matrix metalloproteinase (MMP) inhibitor, on the attenuation of chronic doxorubicin-induced cardiotoxicity in rats. Methods: We allocated male Wistar rats into four groups: control (C), doxorubicin (D), doxycycline (inhibitor of MMP, IM), and Dox + doxycycline (DIM). Groups IM and DIM received doxycycline (5 mg/kg, IP) once a week for 4 weeks. In addition, 48 h after every doxycycline injection, groups D and DIM received Dox (5 mg/kg, IP). We performed echocardiogram and evaluated TIMP-4 and collagen I protein expression, MMP-2 activity, and oxidative stress and myocardial metabolism. Results: Doxorubicin promotes left atrium (LA) and left ventricle (LV) dilatation and decreases in LV fractional shortening, which was improved by doxycycline. Moreover, doxycycline attenuated the LV cardiomyocyte hypertrophy and collagen type I expression. Doxorubicin increased phosphofructokinase and decreased beta-hydroxyacyl Co-A dehydrogenase, pyruvate dehydrogenase, citrate synthase, and ATP synthase activity, which was partially attenuated by doxycycline. Lastly, doxycycline improved antioxidant enzyme activity in the DIM group. Conclusion: Doxorubicin increases oxidative stress and promotes changes in myocardial energy metabolism, accompanied by structural and functional changes. Doxycycline attenuated the doxorubicin-induced cardiotoxicity, at least in part, through changes in myocardial energy metabolism.

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Bast, A., H. Kaiserová, G. J. M. Hartog, G. R. M. M. Haenen, and W. J. F. Vijgh1. "Protectors against doxorubicin-induced cardiotoxicity: Flavonoids." Cell Biology and Toxicology 23, no. 1 (October 24, 2006): 39–47. http://dx.doi.org/10.1007/s10565-006-0139-4.

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AlGhamdi, S., V. Leoncikas, K. E. Plant, and N. J. Plant. "Synergistic interaction between lipid-loading and doxorubicin exposure in Huh7 hepatoma cells results in enhanced cytotoxicity and cellular oxidative stress: implications for acute and chronic care of obese cancer patients." Toxicology Research 4, no. 6 (2015): 1479–87. http://dx.doi.org/10.1039/c5tx00173k.

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Koleini, Navid, Barbara E. Nickel, Andrea L. Edel, Robert R. Fandrich, Amir Ravandi, and Elissavet Kardami. "Oxidized phospholipids in Doxorubicin-induced cardiotoxicity." Chemico-Biological Interactions 303 (April 2019): 35–39. http://dx.doi.org/10.1016/j.cbi.2019.01.032.

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Tao, Zhimin, Henry G. Withers, Harvey S. Penefsky, Jerry Goodisman, and Abdul-Kader Souid. "Inhibition of Cellular Respiration by Doxorubicin." Chemical Research in Toxicology 19, no. 8 (August 2006): 1051–58. http://dx.doi.org/10.1021/tx050315y.

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41

Mohan, Uma Priya, Tirupathi Pichiah P.B., Syeda Thabassum Akhtar Iqbal, and Sankarganesh Arunachalam. "Mechanisms of doxorubicin-mediated reproductive toxicity – A review." Reproductive Toxicology 102 (June 2021): 80–89. http://dx.doi.org/10.1016/j.reprotox.2021.04.003.

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Desai, Varsha G., Vikrant Vijay, Tao Han, Carrie L. Moland, Bounleut Phanavanh, Taewon Lee, Kelly J. Davis, Levan Muskhelishvili, Kimo C. Stine, and James C. Fuscoe. "Doxorubicin‐induced delayed‐onset subclinical cardiotoxicity in mice." Journal of Applied Toxicology 42, no. 5 (October 20, 2021): 778–92. http://dx.doi.org/10.1002/jat.4256.

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43

Bar-Joseph, Hadas, Irit Ben-Aharon, Shulamith Rizel, Salomon M. Stemmer, Moran Tzabari, and Ruth Shalgi. "Doxorubicin-induced apoptosis in germinal vesicle (GV) oocytes☆." Reproductive Toxicology 30, no. 4 (December 2010): 566–72. http://dx.doi.org/10.1016/j.reprotox.2010.07.003.

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44

Gunv�n, Peter, Nils Olof Theve, and Curt Peterson. "Serum and tissue concentrations of doxorubicin after IV administration of doxorubicin or doxorubicin-DNA complex to patients with gastrointestinal cancer." Cancer Chemotherapy and Pharmacology 17, no. 2 (June 1986): 153–56. http://dx.doi.org/10.1007/bf00306745.

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45

Yourtee, David M., Linda L. Elkins, Elisabet L. Nalvarte, and Robert E. Smith. "Amplification of doxorubicin mutagenicity by cupric ion." Toxicology and Applied Pharmacology 116, no. 1 (September 1992): 57–65. http://dx.doi.org/10.1016/0041-008x(92)90144-h.

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Akinjo, Oluwajoba O., Timothy W. Gant, and Emma L. Marczylo. "Perturbation of microRNA signalling by doxorubicin in spermatogonial, Leydig and Sertoli cell lines in vitro." Toxicology Research 7, no. 5 (2018): 760–70. http://dx.doi.org/10.1039/c7tx00314e.

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Doxorubicin-induced testicular toxicity involves perturbation of microRNAs within all three of the main testicular cell types, particularly those involved in germ–Sertoli and Sertoli–Sertoli cell junctions.

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Church, Rachel J., J. Eric McDuffie, Manisha Sonee, Monicah Otieno, Jing Ying Ma, Xuejun Liu, Paul B. Watkins, and Alison H. Harrill. "MicroRNA-34c-3p is an early predictive biomarker for doxorubicin-induced glomerular injury progression in male Sprague-Dawley rats." Toxicol. Res. 3, no. 5 (2014): 384–94. http://dx.doi.org/10.1039/c4tx00051j.

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Increased microRNA-34c-3p appeared as a novel biomarker for doxorubicin nephrotoxicity in rats; alterations showed greater specificity than and comparable sensitivity to albuminuria for early prediction of glomerular injury.

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Akinjo, Oluwajoba O., Timothy W. Gant, and Emma L. Marczylo. "Perturbation of epigenetic processes by doxorubicin in the mouse testis." Toxicology Research 5, no. 4 (2016): 1229–43. http://dx.doi.org/10.1039/c6tx00078a.

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Doxorubicin-induced testicular toxicity involves differential microRNA expression and DNA methylation. This is of potential concern since epigenetic perturbation in the germ line could lead to adverse effects across multiple generations.

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Klimtová, Ivona, Tomáš Šimůnek, Yvona Mazurová, Radomír Hrdina, Vladimír Gerš, and Michaela Adamcová. "Comparative study of chronic toxic effects of daunorubicin and doxorubicin in rabbits." Human & Experimental Toxicology 21, no. 12 (December 2002): 649–57. http://dx.doi.org/10.1191/0960327102ht311oa.

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This study compares the chronic toxicity of two anthracyclines–daunorubicin and doxorubicin, commonly used for induction of anthracycline cardiomyopathy in the rabbit model. Such a comparative study has not been published until now. Both drugs were administered intravenously to male Chinchilla rabbits in doses at 3 mg/ kg (50 mg/m2) once weekly for 10 weeks. Selected biochemical, haematological and cardiovascular parameters and body weights were regularly monitored; additionally, a histological evaluation of heart, kidney and liver was performed at the end of the experiment. In the daunorubicin group, there were marked signs of the progressive development of heart failure, like the significant increases of the pre-ejection period/left ventricular ejection time index values (up to 134%)–and histological changes within the myocardium were also observed. On the other hand, the 10-week doxorubicin administration did not cause these changes that are typical for heart injury. Haematotoxicity, manifested particularly by aplastic anaemia, was apparent in both the experimental groups. Significant body weight loss (by 45.2%) and high premature mortality (100% versus 36.4%) reflected a greater general toxicity, especially nephrotoxicity of doxorubicin in comparison with daunorubicin. Further studies are necessary to find a possible explanation for these findings.

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Hu, B., H. Tan, L. Yu, Q. Liao, and W. Guo. "Repurposing Ivermectin to augment chemotherapy’s efficacy in osteosarcoma." Human & Experimental Toxicology 41 (January 2022): 096032712211436. http://dx.doi.org/10.1177/09603271221143693.

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Background Osteosarcoma is the most frequent malignant bone malignancy and the current treatments are ineffective. Ivermectin, an anti-protozoal drug, has been shown to have anti-cancer activity. This work investigated the potential of repurposing ivermectin to augment chemotherapy’s efficacy in osteosarcoma. Methods Proliferation, migration and apoptosis assays were performed in ivermectin-treated osteosarcoma cells. Combination studies were performed. Osteosarcoma xenograft mouse model was established to investigate the in vivo efficacy of ivermectin. Intracellular reactive oxygen species (ROS) and mitochondrial superoxide, membrane potential, ATP, 8-OHdG level, protein carbonylation and lipid peroxidation were determined after ivermectin treatment. Results Ivermectin was effective and acted synergistically with doxorubicin in osteosarcoma cells regardless of cellular origin and genetic profiling. This was achieved through suppressing inhibiting growth and migration, and inducing caspase-dependent apoptosis. Ivermectin also significantly inhibited osteosarcoma growth in vivo and its combination with doxorubicin resulted in much greater efficacy than doxorubicin alone. Importantly, the effective dose of ivermectin was clinically feasible and did not cause significant toxicity in mice. Mechanistical analysis showed that ivermectin induced oxidative stress and damage, and mitochondrial dysfunction. Conclusions Our findings indicate that ivermectin has utility in treating patients with osteosarcoma, especially those resistant to chemotherapy.

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