Studies on the cytotoxic, biochemical and anti-carcinogenic potentials of ninhydrin on Ehrlich ascites carcinoma cell-bearing swiss albino mice

• Published in: Investigational new drugs 2000-08, Vol.18 (3), p.221-230
• Main Authors: QURESHI, S, AL-SHABANAH, O. A, AL-BEKAIRI, A. M, AL-HARBI, M. M, AL-GHARABLY, N. M, RAZA, M
• Format: Article
• Language: English
• Subjects: Albinism; Animals; Anticarcinogenic Agents - pharmacology; Ascites; Biological and medical sciences; Body Weight - drug effects; Cancer; Carcinogenesis, carcinogens and anticarcinogens; Carcinogens; Carcinoma, Ehrlich Tumor - drug therapy; Carcinoma, Ehrlich Tumor - metabolism; Carcinoma, Ehrlich Tumor - mortality; Cell Survival - drug effects; Chemical agents; Cyclophosphamide - pharmacology; Cytotoxicity; DNA - biosynthesis; Dose-Response Relationship, Drug; Drinking water; Drug dosages; Female; Females; Homeostasis; Laboratories; Malondialdehyde - analysis; Medical sciences; Mice; Ninhydrin - pharmacology; Proteins; Reagents; Sulfhydryl Compounds - analysis; Tumors
• ISSN: 0167-6997; 1573-0646
• DOI: 10.1023/A:1006465504723

Ninhydrin (2,2-dihydroxy-1,3-indane dione) was evaluated for its antitumor and cytotoxic properties in Ehrlich ascites carcinoma cell (EAC Cell)-bearing mice. The rationale behind this study has been mainly the literature reports of its characteristic interference with DNA synthesis and calcium homeostasis. Antitumor activity was evaluated from the total count and viability of EAC cells in addition to their nucleic acid, protein, non-protein sulfhydryls (NP-SH) and malondialdehyde (MDA) contents. The EAC cell-bearing animals were also observed for the effect on their survival and body weight variations. In addition, the tumors grown at the site of injection were evaluated for histopathological changes. Ninhydrin treatments (5, 10 and 20 mg/kg/day) abate the increase in body weight and advanced the duration of survival in EAC cell-bearing mice. The results on histopathological investigations show retardation in tumor growth, decreased frequency of mitotic figures and hair follicles and an increased necrosis in the tumor by ninhydrin treatment. Our results on cytotoxicity, which demonstrated compression in the number of EAC cells and their viability substantiate these data. The results of biochemical studies on EAC cells exhibit a reduction in the levels of DNA, RNA, proteins and NP-SH with a subsequent increase in the concentrations of MDA after ninhydrin treatment. Inhibition in tumor growth was dose dependently significant with the same dose regimen. The observed cytotoxic and antitumor activity of ninhydrin was comparable to cyclophosphamide. The possible mode of action of ninhydrin-induced cytotoxic and antitumor activity appear to be due to its interference with mitochondrial function resulting in inhibition of DNA synthesis, an effect that is being investigated further.