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Abstract
Cisplatin is one of the most active cytotoxic agents in cancer treatment. To clarify the interaction with mitochondria, we hypothesize that the activities of mitochondrial electron transport chain (ETC) enzymes succinate dehydrogenase (SDH) and cytochrome c oxidase (COX), nucleotide levels, as well as levels of catalase (CAT) enzyme and membrane lipid peroxidation (LPO) can be affected by cisplatin. There was a significant decrease of both SDH and COX activities in the lung, heart, and brain tissues at the 1st day after cisplatin exposure, and the observed decreased levels of adenosine triphosphate (ATP) and adenosine diphosphate (ADP) in comparison with the control could be because of cisplatin-induced mitochondrial dysfunction. The investigations suggested that cisplatin inhibits SDH, COX, and ATP synthase. The higher LPO level in the studied tissues after 1 and 4 days post-exposure to cisplatin compared to control can be inferred to be a result of elevated electron leakage from the ETC, and reactive oxygen species (ROS) can lead to wide-ranging tissue damage such as membrane lipid damage. Consequently, it was observed that capsaicin may have a possible protective effect on ETC impairment caused by cisplatin. The activities of SDH and COX were higher in heart and brain exposed to cisplatin + capsaicin compared to cisplatin groups, while LPO levels were lower. The investigated results in the cisplatin + capsaicin groups suggested that the antioxidant capacity of capsaicin scavenges ROS and prevents membrane destruction.
Highlights
Mitochondria are the energy factories of the cell, and this energy is used in the electron transport chain to pump protons across the inner mitochondrial membrane from the inner matrix to the intermembrane space, and a strong hydrogen concentration gradient is produced [1]
Cis-diammineplatinum(II) dichloride, capsaicin, trichloroacetic acid (TCA), and ascorbic acid were obtained from Sigma (Sigma-Aldrich GmbH, Sternheim, Germany), and thiobarbituric acid (TBA), and H2 O2 were from Merck (Darmstadt, Germany)
We evaluated the activities of electron transport chain (ETC) enzymes such as succinate dehydrogenase (SDH) and cytochrome c oxidase (COX), the levels of adenine nucleotides, the activity of the antioxidant enzyme CAT, and levels of lipid peroxidation (LPO) involved in membrane damage in all studied tissues
Summary
Mitochondria are the energy factories of the cell, and this energy is used in the electron transport chain to pump protons across the inner mitochondrial membrane from the inner matrix to the intermembrane space, and a strong hydrogen concentration gradient is produced [1]. Mitochondrial oxygen metabolism is the dominant source of O2 − that results from incomplete coupling of electrons and H+ with oxygen in the electron transport chain [2]. Toxins, and agents that are used extensively in life induce electron leak in the mitochondria. One such agent is cisplatin, a chemotherapeutic agent widely used for the treatment of several types of cancers (e.g., testicular, ovarian, head and neck, cervical, colon, lung, and brain).
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