Methimazole-induced hypothyroidism causes alteration of the REDOX environment, oxidative stress, and hepatic damage; events not caused by hypothyroidism itself

Cano-Europa, Edgar; Blas-Valdivia, Vanessa; Lopez-Galindo, Gabriel Eduardo; Franco-Colín, Margarita; Pineda-Reynoso, Marisol; Hernández-García, A.; Ortiz-Butrón, Rocı́o

doi:10.1016/s1665-2681(19)31684-9

Cited by 26 publications

(22 citation statements)

References 24 publications

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“…Abnormalities in lipid and protein metabolism including enhanced lipolysis and increased breakdown of protein secondary to insulin deficiency may explain the body weight loss observed in streptozotocin-induced diabetes in the present study. Our results are in disagreement with Čakić-Milošević et al (2004) and Cano-Europa et al (2010) who noticed a decrease in body weight in methimazole-induced hypothyroidism. They attributed this weight loss to damaging toxic effects of methimazole or retarded growth due to thyroid hormones deficiency.…”

Section: Discussioncontrasting

confidence: 99%

Impacts of the coexistence of diabetes and hypothyroidism on body weight gain, leptin and various metabolic aspects in albino rats

Ahmed

Gabar

Ali

2012

Journal of Diabetes and its Complications

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Section: Discussioncontrasting

confidence: 99%

Impacts of the coexistence of diabetes and hypothyroidism on body weight gain, leptin and various metabolic aspects in albino rats

Ahmed

Gabar

Ali

2012

Journal of Diabetes and its Complications

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“…In the current study, T3 and T4 concentration decreased in hypothyroidism induced by thyroidectomy and methimazole treated group compared with the euthyroid group. This agreed with Gazia [26], Cano-Europ et al, [38] and Cano-Europa et al, [39] who reported that the concentration of T3 and T4 decreased in the thyroidectomized group and methimazole-treated group.…”

Section: Discussionsupporting

confidence: 91%

samar.zag1234@gmail.com

Khatab¹,

Hulail²,

Hegazy³

et al. 2018

Zagazig University Medical Journal

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Kidney and thyroid functions interact with each other. Drugs used in treatment of any of them could have side reactions on any other organ. The effects of antithyroid medications on extrathyroidal organs could be due to oxidative stress and to damage in the renal cells. Aim: This work is designed to demonstrate the role of T4 in protection against the increase in oxidative stress caused by methimazole, and to detect if antithyroid drug-induced hypothyroidism (methimazole) or removal of thyroid by surgery causes damage of kidney cells or not. Methods: Twenty-five healthy adult male albino rats were used in the study. The animals were randomly separated into groups. Each group contained five rats: Group I (control group): This group received no drugs or treatment. Group II included rats with false thyroidectomy. Group III included thyroidectomized albino rats. Group IV included methimazole-induced hypothyroidism albino rats through receiving 60 mg/kg/day of methimazole in drinking water. Group V were administered methimazole (60 mg/kg/day) and l-thyroxine (T4) subcutaneous injection (20 μg/kg/day).The animals were anasethized and their abdomens were opened and both kidneys were removed, and immediately processed for histological & immunohistochemical study. Also oxidative enzymes were estimated. Rresults: Light microscopic examination of H&E stained sections showed marked damage of the structure of renal cortex in methimazole induced hypothyroidism group. This damage was concomitant with a decrease in kidney antioxidant enzymes. This damage was less pronounced in group of rats administrated T4 in association with methimazole. The cortex of kidney in rats of thyroidectomized group did not show any alterations in its micro structure. Conclusion: Methimazole causes both of hypothyroidism and alteration of the kidney cortex. This alteration is not noticed in case of surgical thyroidectomy inducing hypothyroidism. L-Thyroxine (T4) could decrease the effect of methimazole on kidney cortex.

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“…Modulation of thyroid hormone signaling was achieved using the small molecular inhibitor MMI. After the measurement of EtOH intake for 3 d, both groups of WSR mice (e.g., control and repeated 72 h EtOH vapor) were injected with MMI (i.p., 60 mg/kg/d; daily for 5d) to inhibit thyroid hormone production and induce hypothyroidism (Cano-Europa et al, 2010). The effect on voluntary EtOH consumption was evaluated daily.…”

Section: Methodsmentioning

confidence: 99%

Importance of genetic background for risk of relapse shown in altered prefrontal cortex gene expression during abstinence following chronic alcohol intoxication

et al. 2011

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Alcoholism is a relapsing disorder associated with excessive consumption after periods of abstinence. Neuroadaptations in brain structure, plasticity and gene expression occur with chronic intoxication but are poorly characterized. Here we report identification of pathways altered during abstinence in prefrontal cortex, a brain region associated with cognitive dysfunction and damage in alcoholics. To determine the influence of genetic differences, an animal model was employed with widely divergent responses to alcohol withdrawal, the Withdrawal Seizure-Resistant (WSR) and Withdrawal Seizure-Prone (WSP) lines. Mice were chronically exposed to highly intoxicating concentrations of ethanol and withdrawn, then left abstinent for 21 days. Transcriptional profiling by microarray analyses identified a total of 562 genes as significantly altered during abstinence. Hierarchical cluster analysis revealed that the transcriptional response correlated with genotype/withdrawal phenotype rather than sex. Gene Ontology category overrepresentation analysis identified thyroid hormone metabolism, glutathione metabolism, axon guidance and DNA damage response as targeted classes of genes in low response WSR mice, with acetylation and histone deacetylase complex as highly dimorphic between WSR and WSP mice. Confirmation studies in WSR mice revealed both increased neurotoxicity by histopathologic examination and elevated T3 levels. Most importantly, relapse drinking was reduced by inhibition of thyroid hormone synthesis in dependent WSR mice compared to controls. These findings provide in vivo physiological and behavioral validation of the pathways identified. Combined, these results indicate a fundamentally distinct neuroadaptive response during abstinence in mice genetically selected for divergent withdrawal severity. Identification of pathways altered in abstinence may aid development of novel therapeutics for targeted treatment of relapse in abstinent alcoholics.

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Methimazole-induced hypothyroidism causes alteration of the REDOX environment, oxidative stress, and hepatic damage; events not caused by hypothyroidism itself

Cited by 26 publications

References 24 publications

Impacts of the coexistence of diabetes and hypothyroidism on body weight gain, leptin and various metabolic aspects in albino rats

Impacts of the coexistence of diabetes and hypothyroidism on body weight gain, leptin and various metabolic aspects in albino rats

samar.zag1234@gmail.com

Importance of genetic background for risk of relapse shown in altered prefrontal cortex gene expression during abstinence following chronic alcohol intoxication

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