SLC25A35 Inhibitors

SLC25A35 inhibitor chemicals such as rotenone and antimycin A exert their effects by binding to and inhibiting components of the electron transport chain, leading to a disruption of the mitochondrial membrane potential. This impact on the electrochemical gradient across the mitochondrial membrane is a key factor for the translocation of substrates by carrier proteins like SLC25A35. Oligomycin and the uncouplers CCCP and DNP interfere with the process of oxidative phosphorylation, either by inhibiting ATP synthase or by dissipating the proton gradient. This disruption can lead to changes in ATP production and the mitochondrial membrane potential, both of which are crucial for the activity of mitochondrial carriers.

Furthermore, chemicals that affect the transport of critical substrates across the mitochondrial membrane, such as atractyloside and bongkrekic acid, which inhibit the ADP/ATP translocase, can alter the adenine nucleotide concentrations within the mitochondrial matrix. This alteration can impact the energy balance within the mitochondria, potentially affecting the function of SLC25A35. Valinomycin, by forming potassium channels, disrupts the ionic balance, which can influence the mitochondrial membrane potential and, consequently, mitochondrial carrier activity. Zinc pyrithione, iodoacetate, and α-cyano-4-hydroxycinnamic acid affect mitochondrial function by disrupting ion homeostasis, glycolytic ATP production, and mitochondrial substrate transport, respectively. These disruptions can lead to a decrease in the energy supply or an imbalance in substrate concentrations, which can indirectly affect the functionality of SLC25A35. Lastly, azide targets the terminal component of the electron transport chain, which is essential for maintaining the mitochondrial membrane potential and the associated driving force for substrate transport by carrier proteins like SLC25A35.