Taurine prevents mitochondrial membrane permeabilization and swelling upon interaction with manganese: Implication in the treatment of cirrhosis-associated central nervous system complications.
Nahid AhmadiVahid GhanbarinejadMohammad Mehdi OmmatiAkram JamshidzadehReza HeidariPublished in: Journal of biochemical and molecular toxicology (2018)
Brain tissue manganese (Mn) accumulation is a cirrhosis-associated complication. Cellular mitochondria are among the potential targets for Mn-induced cytotoxicity. Taurine is one of the most abundant amino acids with high concentrations in human brain tissue. Several pharmacological properties including regulation of mitochondrial function are attributed to taurine. The current investigation was designed to evaluate the effect of taurine on Mn-induced mitochondrial impairment in isolated mice brain mitochondria. The brain mitochondria were exposed to increasing concentrations of Mn (0.1-10 mM). Taurine (0.1, 1, and 10 mM) was added as the protective agent. The severe collapse of mitochondrial membrane potential, decreased mitochondrial dehydrogenases activity, mitochondrial swelling, and depleted mitochondrial adenosine triphosphate (ATP) were evident in Mn-exposed mitochondria. It was found that taurine administration preserved mitochondrial ATP, prevented mitochondrial depolarization and swelling, and increased mitochondrial dehydrogenases activity. These data suggest mitochondrial protection as an underlying mechanism for the protective effects of taurine against Mn toxicity.
Keyphrases
- oxidative stress
- diabetic rats
- cell death
- room temperature
- type diabetes
- resting state
- metabolic syndrome
- machine learning
- white matter
- drug induced
- brain injury
- risk factors
- amino acid
- insulin resistance
- functional connectivity
- adipose tissue
- skeletal muscle
- artificial intelligence
- mouse model
- blood brain barrier
- early onset
- cerebrospinal fluid