Key result
Doxorubicin drives nearly 2-fold higher cardiac oxidative stress than controls, exceeding cisplatin cardiotoxicity.
Why the study?
Doxorubicin and cisplatin are widely used chemotherapeutic drugs whose clinical use is limited by systemic and organ-specific toxicities that require comparative evaluation.
Absolute Event Rate: 24.44% vs 13.02%
p-value: p=<0.001
Doxorubicin and cisplatin administered at identical doses both induce significant multi-organ toxicity through oxidative stress, inflammation, and apoptosis, but doxorubicin produces markedly more severe cardiac and splenic injury.
May warrant preferential cisplatin consideration in high cardiac-risk patients; animal data extends comparative toxicity profiles but leaves clinical translation open.
Doxorubicin (DOX) and cisplatin (CIS) are extensively used chemotherapeutic drugs, but their clinical use is hindered by systemic and organ-specific toxicities. This study comparatively evaluated the oxidative, inflammatory, hematological, immune, and tissue responses induced by DOX and CIS administered at the same dose. Adult male albino rats were randomly allocated into control and chemotherapy-treated groups. The chemotherapy groups received a single intraperitoneal injection of DOX or CIS (7.5 mg/kg). Serum oxidative stress markers (malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH)), inflammatory markers (tumor necrosis factor-alpha, interleukin-6, and myeloperoxidase), lactate dehydrogenase (LDH), troponin T, immunoglobulins (IgG and IgM), and hematological parameters were assessed. Cardiac and splenic tissues were evaluated for MDA, SOD, Nuclear factor kappa B (NF-κB), and caspase-3, together with histopathological examination and scoring. Both DOX and CIS caused anemia, leukocyte imbalance, thrombocytosis, and increased IgG and IgM, with more severe effects in DOX. Both agents also induced systemic oxidative stress, inflammation, and increased LDH and troponin T levels. In cardiac and splenic tissues, these treatments were associated with increased MDA, NF-κB, and caspase-3 levels, with reduced SOD activity. Histopathological examination and scoring revealed myocardial degeneration, vacuolation, necrosis, and inflammatory infiltration, as well as splenic white pulp depletion and disruption of the red–white pulp boundaries, with more pronounced damage observed in the DOX group. DOX and CIS induced systemic and tissue oxidative, inflammatory, hematological, and apoptotic disturbances, supporting an oxidative stress–NF-κB–apoptosis pathway in cardiac and splenic toxicity.
No takes yet. Share an insight, caveat, or question.
Badr et al. (2026) studied Chemotherapy-induced toxicity (n=15). Doxorubicin and Cisplatin vs. Control was evaluated on Cardiac tissue malondialdehyde (MDA) levels (nmol/g tissue) for DOX vs Control (p=<0.001). Both doxorubicin and cisplatin induced systemic and tissue oxidative, inflammatory, and apoptotic disturbances, with doxorubicin causing more severe cardiac and splenic damage.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: