Due to the present renewable fuels demand increase, reduction of second-generation bioethanol production cost is pursued, since it is considered the most promising biofuel, but not yet economically viable. A proposed solution is its production through a simultaneous saccharification and fermentation process (SSF); however, it is necessary to apply temperatures above 40°C, which reduce the viability of traditional ethanologenic yeasts. As consequence, the use of thermotolerant ethanologenic yeast has been suggested, among which the yeast Kluyveromyces marxianus stands out. This chapter addresses the production of second-generation bioethanol through the SSF process, emphasizing the potential of K. marxianus to transform lignocellulosic biomass as agave bagasse. As result, it is proposed to direct the second-generation bioethanol production to the SSF process employing thermotolerant yeasts, to increase process productivity, and addressing the economic barriers.
Part of the book: Special Topics in Renewable Energy Systems
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.
Part of the book: Antioxidants