ArticleScientific reports2017
Nitric oxide mediates apoptosis and mitochondrial dysfunction and plays a role in growth hormone deficiency by nivalenol in GH3 cells.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Growth hormone alleviates oxidative stress and improves oocyte quality in Chinese women with polycystic ovary syndrome: a randomized controlled trial.Scientific reports · 2020Trial
- Early Cardiovascular and Metabolic Benefits of rhGH Therapy in Adult Patients with Severe Growth Hormone Deficiency: Impact on Oxidative Stress Parameters.International journal of molecular sciences · 2025Article
- Impact of Genotropin on Oxidative Stress, Glutamate, and Nitric Oxide Pathways in a Rat Model of Peripheral Neuropathy.Basic and clinical neuroscience · 2025Article
- Growth Hormone Promotes Oocyte Maturation In Vitro by Protecting Mitochondrial Function and Reducing Apoptosis.Reproductive sciences (Thousand Oaks, Calif.) · 2023Article
- An update on T2-toxins: metabolism, immunotoxicity mechanism and human assessment exposure of intestinal microbiota.Heliyon · 2022Review
- Architects of Pituitary Tumour Growth.Frontiers in endocrinology · 2022Review
- MicroRNA-294 Regulates Apoptosis of the Porcine Cerebellum Caused by Selenium Deficiency via Targeting iNOS.Biological trace element research · 2021Article
- The Antitumor Efficacy ofBioMed research international · 2020Review
- Mitochondrial Dysfunction Pathway Networks and Mitochondrial Dynamics in the Pathogenesis of Pituitary Adenomas.Frontiers in endocrinology · 2019Review
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8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nivalenol (NIV), a type B trichothecenes commonly found in cereal crops, can cause growth impairment in animals. However, limited information about its mechanisms is available. Trichothecenes have been characterized as an inhibitor of protein synthesis and induce apoptosis in cells. Oxidative stress is considered an underlying mechanism. However, whether NIV can induce oxidative stress and apoptosis in rat pituitary cells line GH3 is unclear. The present study showed that NIV significantly reduced the viability of cells and caused oxidative stress in GH3 cells. Further experiments showed that nitric oxide (NO), but not ROS, mediated NIV-induced oxidative stress. Additionally, NIV induced caspase-dependent apoptosis, decrease in mitochondrial membrane potential and mitochondrial ultrastructural changes. However, NIV-induced caspase activation, mitochondrial damage and apoptosis were partially alleviated by Z-VAD-FMK or NO scavenger hemoglobin. Finally, NIV changed the expression of growth-associated genes and pro-inflammatory cytokines. NIV also reduced the GH secretion in GH3 cells, which was reversed by hemoglobin. Taken together, these results suggested that NIV induced apoptosis in caspase-dependent mitochondrial pathway in GH3 cells, which might be an underlying mechanism of NIV-induced GH deficiency. Importantly, NO played a critical role in the induction of oxidative stress, apoptosis and GH deficiency in NIV-treated GH3 cells.
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