ArticleThe journals of gerontology. Series A, Biological sciences and medical sciences2014
Growth hormone alters the glutathione S-transferase and mitochondrial thioredoxin systems in long-living Ames dwarf mice.
Article in The journals of gerontology. Series A, Biological sciences and medical sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Thioredoxin (Trx): A redox target and modulator of cellular senescence and aging-related diseases.Redox biology · 2024Review
- Integrated metabolomics reveals altered lipid metabolism in adipose tissue in a model of extreme longevity.GeroScience · 2020Article
- Effects of GH/IGF on the Aging Mitochondria.Cells · 2020Review
- Cytoplasmic and Mitochondrial NADPH-Coupled Redox Systems in the Regulation of Aging.Nutrients · 2019Review
- Mitochondrial Function Is Compromised in Cortical Bone Osteocytes of Long-Lived Growth Hormone Receptor Null Mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2019Article
- Age-associated changes in GSH S-transferase gene/proteins in livers of rats.Redox report : communications in free radical research · 2018Article
- Evidence that growth hormone can improve mitochondrial function in oocytes from aged mice.Reproduction (Cambridge, England) · 2018Article
- Metabolic adaptation of short-living growth hormone transgenic mice to methionine restriction and supplementation.Annals of the New York Academy of Sciences · 2018Article
- Insulin-like growth factor receptor signaling regulates working memory, mitochondrial metabolism, and amyloid-β uptake in astrocytes.Molecular metabolism · 2018Article
- Growth Hormone (GH) and Cardiovascular System.International journal of molecular sciences · 2018Review
- Energy metabolism and inflammation in brain aging and Alzheimer's disease.Free radical biology & medicine · 2016Review
- Growth hormone treatment of premature ovarian failure in a mouse model via stimulation of the Notch-1 signaling pathway.Experimental and therapeutic medicine · 2016Article
- Reduced growth hormone signaling and methionine restriction: interventions that improve metabolic health and extend life span.Annals of the New York Academy of Sciences · 2016Review
- The somatotropic axis and longevity in mice.American journal of physiology. Endocrinology and metabolism · 2015Review
- Fibroblasts derived from long-lived insulin receptor substrate 1 null mice are not resistant to multiple forms of stress.Aging cell · 2014Article
- Altered dietary methionine differentially impacts glutathione and methionine metabolism in long-living growth hormone-deficient Ames dwarf and wild-type mice.Longevity & healthspan · 2014Article
- Effects of insulin-like growth factor 1 on glutathione S-transferases and thioredoxin in growth hormone receptor knockout mice.Age (Dordrecht, Netherlands) · 2014Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Ames dwarf mice are deficient in growth hormone (GH), prolactin, and thyroid-stimulating hormone and live significantly longer than their wild-type (WT) siblings. The lack of GH is associated with stress resistance and increased longevity. However, the mechanism underlying GH's actions on cellular stress defense have yet to be elucidated. In this study, WT or Ames dwarf mice were treated with saline or GH (WT saline, Dwarf saline, and Dwarf GH) two times daily for 7 days. The body and liver weights of Ames dwarf mice were significantly increased after 7 days of GH administration. Mitochondrial protein levels of the glutathione S-transferase (GST) isozymes, K1 and M4 (GSTK1 and GSTM4), were significantly higher in dwarf mice (Dwarf saline) when compared with WT mice (WT saline). GH administration downregulated the expression of GSTK1 proteins in dwarf mice. We further investigated GST activity from liver lysates using different substrates. Substrate-specific GST activity (bromosulfophthalein, dichloronitrobenzene, and 4-hydrox-ynonenal) was significantly reduced in GH-treated dwarf mice. In addition, GH treatment attenuated the activity of thioredoxin and glutaredoxin in liver mitochondria of Ames mice. Importantly, GH treatment suppressed Trx2 and TrxR2 mRNA expression. These data indicate that GH has a role in stress resistance by altering the functional capacity of the GST system through the regulation of specific GST family members in long-living Ames dwarf mice. It also affects the regulation of thioredoxin and glutaredoxin, factors that regulate posttranslational modification of proteins and redox balance, thereby further influencing stress resistance.
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