Curcumin Mitigates Streptozotocin-Induced Genotoxicity In Vivo by Activating P53 Protein and Inhibiting Oxidative Stress and Chromosomal Aberration.

Abstract

Genotoxins are chemical constituents that damage DNA or chromosomal architecture, leading to alterations in the genetic level. Streptozotocin, a monofunctional nitrosourea derivative, is often utilized to induce diabetes mellitus in laboratory animals because of its detrimental effects on pancreatic cells. The purpose of this work was to investigate possible protective efficacy against the genotoxic effects of Streptozotocin. This study examines the potentiality of curcumin, a phytoproduct with anti-genotoxic and anti-diabetic qualities, against streptozotocin-induced chromosomal abnormalities and DNA damage. The study evaluates the possible protective efficacy of curcumin, exploring a variety of biochemical and molecular biology techniques in murine models. The experiment involves a control group, the administration of Streptozotocin (Group S), and a curcumin-pretreated STZ group (Group SC) in mice. The effects of curcumin on DNA damage and chromosomal aberrations were investigated by histopathology, immunofluorescence, evaluation of chromosomal aberrations, detection of Reactive oxygen species, cell viability analysis, and DNA laddering assay. The results demonstrated a significant reduction in DNA damage, chromosomal anomalies, and a decrease in the expression of the p53 protein in the curcumin-treated animals compared to that of STZ-treated mice. The overall results show that curcumin can reduce chromosomal aberrations and DNA damage by altering the expression of p53 repair proteins. This suggests that curcumin has a promising future as a therapeutic agent, especially when it comes to drug-induced toxicity and the development of novel therapeutics.