Acute toxic effects of 3,3′-iminodipropionitrile on hypothalamic-pituitary-gonadal axis in male rats

Takahashi, Noriyuki; Hamada, Naomi; Ishizuka, Bunpei

doi:10.1016/j.reprotox.2013.10.007

Cited by 3 publications

(2 citation statements)

References 25 publications

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“…It is effective in establishing the TS model (Zhang & Li, 2015). However, the toxicity of IDPN can act on systemic organs and tissues (not only neural system) (Boadas‐Vaello et al., 2017; Takahashi et al., 2012, 2014). Therefore, the necrotic tissues/cells may activate the immune response and induce the expression of inflammatory cytokines (e.g., IL‐1β, IL‐6, and TNF‐α) as well (Alwelaie et al., 2019).…”

Section: Discussionmentioning

confidence: 99%

Immune function changes of the IDPN‐induced Tourette syndrome rat model

Liu

Wang²,

2021

Intl J of Devlp Neuroscience

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There may be immunologic alternations during Tourette syndrome (TS) development. This study aimed to determine the immune function changes in different aspects (spleen or thymus index, plasma cytokines, and T cell) in an 3,3′‐iminodipropionitrile (IDPN)‐induced rat model of TS. Male Sprague‐Dawley rats were assigned to control and TS groups. The control group received intraperitoneal infections of normal saline (5 ml kg−1 day−1), and the TS rats were injected with IDPN (150 mg kg−1 day−1). The spleen and thymus indices were calculated. The expression of anti‐inflammatory cytokines and inflammatory cytokines TNF‐α, in peripheral blood were measured by ELISA and Western blotting. The proportion of CD3+, CD4+, CD8+, Treg, Th1, and Th2 cells were determined by fluorescence‐activated cell sorting analysis. After 1 week of IDPN treatment, TS rats had decreased spleen and thymus weights versus control. The plasma levels of IL‐4, IL‐10, IL‐12, IFN‐γ, and TNF‐α were significantly increased, while no significant difference in TGF‐β was found. Flow cytometry analysis demonstrated that TS rats had significantly reduced CD3+ and CD4+ cells in spleen, without any change in the proportion of CD8+ cells. Furthermore, the ratio of Treg cells (CD4+/CD25+/FoxP3+) was decreased in TS rats; simultaneously, Th1 cells (CD4+/IFN‐γ+) and Th2 cells (CD4+/IL4+) were dramatically increased. Together, IDPN can trigger immune dysfunction through impairment of matured Th cells, in particular for the Treg subset.

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Section: Discussionmentioning

confidence: 99%

Immune function changes of the IDPN‐induced Tourette syndrome rat model

Liu

Wang²,

2021

Intl J of Devlp Neuroscience

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“…Thus, a limitation of this study and of the IDPNvestibular injury model is that IDPN has additional effects that raise the possibility of complex systemic interactions during IDPN exposure. For example, IDPN treatment of rats is reported to increase apoptosis as indicated by Caspase 3 immunolabeling in anterior pituitary cells and in spermatids 4-8 days after treatment (Takahashi et al 2014). Another study reports histopathological changes in the kidney and liver by day 9 after IDPN treatment in mice (Khan and Ibrahim 2015).…”

Section: Discussionmentioning

confidence: 99%

Effects of 3,3′-Iminodipropionitrile on Hair Cell Numbers in Cristae of CBA/CaJ and C57BL/6J Mice

Wilkerson

Artoni

Lea

et al. 2018

JARO

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This study examines absolute hair cell numbers in the cristae of C57BL/6J mice and CBA/CaJ mice from weaning to adulthood as well as the dose required for 3,3'-iminodiproprionitrile (IDPN)-injury of the cristae in C57BL/6J mice and CBA/CaJ mice, the two mouse strains most commonly used by inner ear researchers. In cristae of CBA/CaJ and C57BL/6J mice, no loss of hair cells was observed up to 24 weeks. In both strains, dose-dependent loss of hair cells was observed 7 days after IDPN treatment of 2-month-old mice (IC = 16.1 mmol/kg in C57BL/6J mice vs. 25.21 mmol/kg in CBA/CaJ mice). Four-month-old C57BL/6J mice exposed to IDPN developed dose-dependent vestibular dysfunction as indicated by increased activity and circling behavior in open field tests and by failure to swim 7 days after treatment. IDPN-hair cell injury in C57BL/6J mice and CBA/CaJ mice represents a fast and predictable experimental model for the study of vestibular degeneration and a platform for the testing of vestibular therapies.

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Gastrodin Attenuates Cognitive Deficits Induced by 3,3′-Iminodipropionitrile

Wang

Liu

et al. 2016

Neurochem Res

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3,3'-Iminodipropionitrile (IDPN), one of the nitrile derivatives, can induce persistent neurotoxicity, and therefore cause dyskinesia and cognitive impairments. Gastrodin, a main bioactive ingredient of Gastrodia elata Blume, is shown to greatly improve cognitive function. The aim of this study was to further determine whether administration of gastrodin can ameliorate IDPN-induced cognitive deficits in the Morris water maze (MWM) and novel object recognition (NOR) task, and to explore the underlying mechanisms. Results showed that exposure to IDPN (100 mg/kg/day, for 8 days) significantly impaired spatial and object recognition memory and that repeated treatment with gastrodin (150 mg/kg/day, for 6 weeks) could effectively alleviate the IDPN-induced cognitive impairments as indicated by increased spatial memory and discrimination ratio in the MWM and NOR tests. Gastrodin treatment also reverted IDPN-induced decreases of γ-aminobutyric acid (GABA) levels and increases of a2 GABAA receptor protein expression in the prefrontal cortex and hippocampus of IDPN-treated rats. These results suggest that gastrodin treatment may provide a novel pharmacological strategy for IDPN-induced cognitive deficits, which was mediated, at least in part, by normalizing the GABAergic system.

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Acute toxic effects of 3,3′-iminodipropionitrile on hypothalamic-pituitary-gonadal axis in male rats

Cited by 3 publications

References 25 publications

Immune function changes of the IDPN‐induced Tourette syndrome rat model

Immune function changes of the IDPN‐induced Tourette syndrome rat model

Effects of 3,3′-Iminodipropionitrile on Hair Cell Numbers in Cristae of CBA/CaJ and C57BL/6J Mice

Gastrodin Attenuates Cognitive Deficits Induced by 3,3′-Iminodipropionitrile

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