Taurine Rescues Cisplatin-Induced Muscle Atrophy In Vitro: A Morphological Study

Stacchiotti, Alessandra; Rovetta, Francesca; Ferroni, Matteo; Corsetti, Giovanni; Llombart‐Bosch, Antonio; Sberveglieri, G.; Aleo, Maria Francesca

doi:10.1155/2014/840951

Cited by 20 publications

(17 citation statements)

References 52 publications

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“…This, in turn, promotes muscle cell apoptosis or even necrosis. In addition to the action of taurine in oxidative stress, some research shows that taurine reduces the abundance of apoptotic signal proteins or rescues drug‐induced muscle atrophy . Regenerative processes are characterized by cellular cleansing (autophagy) and the formation of new muscle cells (myogenesis) .…”

Section: Biological Functions Of Taurinementioning

confidence: 99%

Taurine: A Regulator of Cellular Redox Homeostasis and Skeletal Muscle Function

Seidel

Huebbe

Rimbach

2018

Molecular Nutrition Food Res

124

118

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Taurine is a nonproteinogenic ß-aminosulfonic acid. Important dietary sources of taurine are fish and seafood. Taurine interacts with ion channels, stabilizes membranes, and regulates the cell volume. These actions confirm its high concentrations in excitable tissues like retina, neurons, and muscles. Retinal degeneration, cardiomyopathy, as well as skeletal muscle malfunction are evident in taurine-deficient phenotypes. There is evidence that taurine counteracts lipid peroxidation and increases cellular antioxidant defense in response to inflammation. In activated neutrophils, taurine reacts with hypochloric acid to form taurine chloramine, which triggers the Kelch-like ECH-associated protein 1-nuclear factor E2-related factor 1 (Keap1-Nrf2) pathway. Consequently, Nrf2 target genes, such as heme oxygenase-1 and catalase, are induced. Furthermore, taurine may prevent an overload of reactive oxygen species (ROS) directly by an inhibition of ROS generation within the respiratory chain. Taurine affects mitochondrial bioenergetics and taurine-deficient mice exhibit an impaired exercise performance. Moreover, some studies demonstrate that taurine enhances the glycogen repletion in the postexercise recovery phase. In the case of taurine deficiency, many studies observed a phenotype known in muscle senescence and skeletal muscle disorders. Overall, taurine plays an important role in cellular redox homeostasis and skeletal muscle function.

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Section: Biological Functions Of Taurinementioning

confidence: 99%

Taurine: A Regulator of Cellular Redox Homeostasis and Skeletal Muscle Function

Seidel

Huebbe

Rimbach

2018

Molecular Nutrition Food Res

124

118

View full text Add to dashboard Cite

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“…(28) Cisplatin, another platinum-based chemotherapy drug, caused a decrease in C2C12 myotube diameter and increased markers of autophagy and apoptosis. (29) Cisplatin also induces muscle atrophy via UPS-mediated protein degradation and decreases in protein kinase B (Akt) and forkhead box O3a (Foxo3a) phosphorylation in mice. (30) Akt dephosphorylation decreases activation of the mammalian target of rapamycin complex 1 (mTORC1) which, in turn, decreases the phosphorylation and subsequent activation of the downstream targets of mTORC1, p70S6k and 4E-BP1.…”

Section: Introductionmentioning

confidence: 99%

Zoledronic Acid Improves Muscle Function in Healthy Mice Treated with Chemotherapy

Hain

Jude

et al. 2019

Journal of Bone and Mineral Research

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Carboplatin is a chemotherapy drug used to treat solid tumors but also causes bone loss and muscle atrophy and weakness. Bone loss contributes to muscle weakness through bone-muscle crosstalk, which is prevented with the bisphosphonate zoledronic acid (ZA). We treated mice with carboplatin in the presence or absence of ZA to assess the impact of bone resorption on muscle. Carboplatin caused loss of body weight, muscle mass, and bone mass, and also led to muscle weakness as early as 7 days after treatment. Mice treated with carboplatin and ZA lost body weight and muscle mass but did not lose bone mass. In addition, muscle function in mice treated with ZA was similar to control animals. We also used the anti-TGFβ antibody (1D11) to prevent carboplatin-induced bone loss and showed similar results to ZA-treated mice. We found that atrogin-1 mRNA expression was increased in muscle from mice treated with carboplatin, which explained muscle atrophy. In mice treated with carboplatin for 1 or 3 days, we did not observe any bone or muscle loss, or muscle weakness. In addition, reduced caloric intake in the carboplatin treated mice did not cause loss of bone or muscle mass, or muscle weakness. Our results show that blocking carboplatin-induced bone resorption is sufficient to prevent skeletal muscle weakness and suggests another benefit to bone therapy beyond bone in patients receiving chemotherapy.n 368 HAIN ET AL. TissueMice were euthanized and the tibialis anterior (TA), soleus, and gastrocnemius were dissected. The extensor digitorum longus (EDL) muscle was dissected for muscle contractility. Muscles were either snap frozen in liquid nitrogen for biochemical analysis or embedded in optimum cutting temperature (O.C.T., Tissue Tek, Torrance, CA, USA) compound in cryomolds and frozen in liquid nitrogencooled 2-methylbutane (isopentane) for histological analysis. (38) Journal of Bone and Mineral Research ZA IMPROVES MUSCLE FUNCTION IN HEALTHY MICE TREATED WITH CHEMOTHERAPY 369 n 40. Wen Y, Murach KA, Vechetti IJ Jr, et al. MyoVision: software for automated high-content analysis of skeletal muscle immunohistochemistry. J Appl Physiol. 2018;124(1):40-51. 41. Edwards JR, Nyman JS, Lwin ST, et al. Inhibition of TGF-beta signaling by 1D11 antibody treatment increases bone mass and quality in vivo.

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“…However, although taurine supplementation helped restore muscle function, it did not prevent muscle atrophy in this model (155). Alternatively, pretreatment of C2C12 mouse myotubes with taurine counteracted muscle atrophy and restored mitochondrial function when the myotubes were exposed to cisplatin, a pharmacological inducer of muscle weakness and cachexia (156).…”

Section: Taurinementioning

confidence: 80%

Amino acids in healthy aging skeletal muscle

2016

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Life expectancy in the U.S. and globally continues to increase. Despite increased life expectancy quality of life is not enhanced, and older adults often experience chronic age-related disease and functional disability, including frailty. Additionally, changes in body composition such as the involuntary loss of skeletal muscle mass (i.e. sarcopenia) and subsequent increases in adipose tissue can augment disease and disability in this population. Furthermore, increased oxidative stress and decreased antioxidant concentrations may also lead to metabolic dysfunction in older adults. Specific amino acids, including leucine, cysteine and its derivative taurine, and arginine can play various roles in healthy aging, especially in regards to skeletal muscle health. Leucine and arginine play important roles in muscle protein synthesis and cell growth while cysteine and arginine play important roles in quenching oxidative stress. Evidence suggests that supplemental doses of each of these amino acids may improve the aging phenotype. However, additional research is required to establish the doses required to achieve positive outcomes in humans.

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Taurine Rescues Cisplatin-Induced Muscle Atrophy In Vitro: A Morphological Study

Cited by 20 publications

References 52 publications

Taurine: A Regulator of Cellular Redox Homeostasis and Skeletal Muscle Function

Taurine: A Regulator of Cellular Redox Homeostasis and Skeletal Muscle Function

Zoledronic Acid Improves Muscle Function in Healthy Mice Treated with Chemotherapy

Amino acids in healthy aging skeletal muscle

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