Anthracycline-based combined chemotherapy in the mouse model.

Area of Science:

• Biochemistry
• Pharmacology
• Toxicology

Background:

• Anthracycline-based chemotherapy (doxorubicin, vincristine, prednisolone - DVP) can cause cytotoxicity.
• Investigating protective agents against chemotherapy-induced toxicity is crucial for improving patient outcomes.

Purpose of the Study:

• To evaluate the effects of selenium (Se) ion, N-acetylcysteine (NAC), sodium salt of monoketocholic acid (MKH), and superoxide dismutase (SOD) on DVP chemotherapy-induced cytotoxicity in an experimental animal model.
• To assess the impact of these agents on key biochemical parameters related to oxidative stress.

Main Methods:

• Administration of Se, NAC, MKH, and SOD in an experimental animal model.
• Assessment of lipid peroxidation (LPx) levels.
• Measurement of peroxidase (Px), catalase (CAT), glutathione-peroxidase (GSHPx), and xanthine-oxidase (XOD) enzyme activities.

Main Results:

• SOD, MKH, DVPSe, and DVPMKH significantly increased LPx activity.
• All chemotherapeutic agents (DVP) significantly reduced Px activity.
• DVP, SOD, MKH, DVPSOD, DVPSe, and DVPMKH significantly reduced XOD activity, with MKH showing the lowest activity.
• NAC, Se, DVP, MKH, and DVPMKH reduced CAT activity, while DVPSOD and DVPSe increased it.

Conclusions:

• The tested agents (Se, NAC, MKH, SOD) exhibit varied effects on biochemical parameters associated with DVP chemotherapy.
• Some agents may modulate oxidative stress markers, indicating a complex interaction with chemotherapy-induced cytotoxicity.
• Further research is needed to elucidate the precise mechanisms and therapeutic potential of these agents in mitigating DVP toxicity.