The Protective Effect of Berberis aristata against Mitochondrial Dysfunction Induced due to Co-administration of Mitomycin C and Cisplatin
- *Corresponding Author:
- Dr. Kavita Kumari K
Current Affiliation: Jawaharlal Nehru Institute of Advanced Studies (JNIAS)
6th Floor, Buddha Bhawan, MG Road, Secunderabad-500003
Andhra Pradesh, India
E-mail: [email protected]
Received Date: June 04, 2012; Accepted Date: July 07, 2012; Published Date: July 09, 2012
Citation: Kavita Kumari K, Setty OH (2012) The Protective Effect of Berberis aristata against Mitochondrial Dysfunction Induced due to Co-administration of Mitomycin C and Cisplatin. J Cancer Sci Ther 4:199-206. doi:10.4172/1948-5956.1000142
Copyright: © 2012 Kavita Kumari K, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Background: The combination of mitomycin C and cisplatin was proved to be beneficial in the treatment of lung cancer, breast cancer, anal carcinoma and human cervical cancer treatment. However, dose related toxicity happens to be one of the major concerns the treatment, leading to its discontinuation, although the patient’s response is encouraging. The aim of the present investigation was to study the protective effects of Berberis aristata (10 mg/kg body weight) on the mitochondrial dysfunction caused due to administration of mitomycin C (2 mg/kg body wt, i.p) and cisplatin (12 mg/kg body wt, i.p).
Methods: We have investigated the effects and protective effects on oxidative phosphorylation enzymes, of the electron transport system, lipid peroxidation and phospholipid composition in liver and kidney mitochondria.
Results: Co-administration of mitomycin C and cisplatin resulted in significant decrease in active respiration (State 3 Respiration), Respiratory Control Ratio (RCR) and P/O ratio’s using either succinate or glutamate plus malate as substrate. Altered enzyme activities of NADH dehydrogenase, succinate dehydrogenase, succinatecytochrome c reductase, NADH-cytochrome c reductase, cytochrome c oxidase was observed. The level of lipid peroxides was increased, and with a significant decrease in phospholipid content. Prior administration of Berberis aristata protected against observed mitochondrial dysfunction.
Conclusions: We believe that prior administration of Berberis aristata could reduce the damage to mitochondrial function, by scavenging free radicals and thereby, preventing uncoupling of oxidative phosphorylation, deactivation of enzymes of electron transport chain, generation of lipid peroxides, oxidation of phospholipids ultimately inhibiting the signaling wave propagation to the mitochondria death receptor (membrane bound cytochrome c), which generally leads to apoptosis.