Histone H1 modulates the antioxidant status in 9,10-dimethylbenz[a]anthracene-induced experimental breast cancer

Oxidative stress is implicated in the pathogenicity of cancer cells and contributes towards the response to antineoplastic agents. This study was aimed at assessing the antioxidant status in 9,10-dimethylbenz[a]anthracene-induced experimental animals treated with histone H1.

Histone H1 was injected and the antioxidant status was assessed in erythrocytes and tumour tissue of experimental animals. The antioxidant status was monitored from the levels of lipid peroxides as thiobarbituric acid reactants and conjugated dienes in the haemolysate, serum, glutathione, and plasma vitamins A, E, C and ceruloplasmin. In the haemolysate, activities of antioxidant enzymes, including superoxide dismutase, catalase, glutathione reductase, gamma-glutamyl transpeptidase, glutathione S-transferase, glutathione peroxidase and glucose-6-phosphate dehydrogenase, were assayed and erythrocyte fatty acid composition was analyzed by gas chromatography-mass spectrometry. All of the above parameters except fatty acid composition were assessed within the tumour tissue to assess the antioxidant status.

Treatment with histone H1 enhanced the antioxidant in erythrocyte at the end of the 2nd and 4th week by significantly decreasing thiobarbituric acid-reactive substances and conjugated dienes, by increasing glutathione levels, activities of antioxidant enzymes and favourably altering the erythrocyte fatty acid composition. Within the tumour tissue, a significant atrophy with significant alteration in antioxidant and antioxidant enzyme status was evident in treatment.

These results validate the role of histone H1 as an antitumour agent in breast cancer.