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Thiol Reduction And Cardiolipin Improve Complex I Activity And Free Radical Production In Liver Mitochondria Of Streptozotocin-Induced Diabetic Rats

Manjury Jatziry Hernández-Esparza, Claudia Guadalupe Flores-Ledesma, Rocío Montoya-Pérez, Elizabeth Calderón-Cortés, Alfredo Saavedra-Molina, Alain Raimundo Rodríguez-Orozco, Christian Cortés-Rojo

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Mitochondrial reactive oxygen species (ROS) are involved in diabetic liver disease development. Diabetes impairs complex I activity and increases ROS production in liver mitochondria. The complex I produces ROS in forward electron transfer (FET) or in reverse electron transfer (RET) modes depending on the site of electron transfer blocking and the availability of respiratory substrates. Complex I activity depends on the phospholipid cardiolipin and the redox state of reactive thiols in the enzyme. Neither the underlying factors leading to complex I dysfunction nor the mode of ROS production have been elucidated in liver mitochondria in diabetes. We tested in liver mitochondria from streptozotocin (STZ) -induced diabetic rats if the addition of cardiolipin or β-mercaptoethanol, a thiol reducing agent, recovers complex I activity and decreases ROS production with substrates inducing ROS production in FET or RET modes. Decreased complex I activity and enhanced ROS generation in FET mode was detected in mitochondria from diabetic rats. Complex I activity was fully restored with the combined treatment with cardiolipin plus β-mercaptoethanol, which also abated ROS generation in FET mode. This suggest that therapies restoring cardiolipin and reducing mitochondrial thiols might be useful to counteract impaired complex I activity and excessive ROS production in liver mitochondria in diabetes.