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Thyroid redox imbalance in adult Wistar rats that were exposed to nicotine during breastfeeding.

ABSTRACT: Maternal nicotine exposure causes several consequences in offspring phenotype, such as obesity and thyroid dysfunctions. Nicotine exposure can increase oxidative stress levels, which could lead to thyroid dysfunction. However, the mechanism by which nicotine exposure during breastfeeding leads to thyroid gland dysfunction remains elusive. We aimed to investigate the long-term effects of maternal nicotine exposure on redox homeostasis in thyroid gland, besides other essential steps for thyroid hormone synthesis in rats from both sexes. Lactating Wistar rats were implanted with osmotic minipumps releasing nicotine (NIC, 6 mg/kg/day) or saline (control) from postnatal day 2 to 16. Offspring were analyzed at 180-day-old. NIC males showed lower plasma TSH, T3 and T4 while NIC females had higher T3 and T4. In thyroid, NIC males had higher sodium-iodide symporter protein expression, whereas NIC females had higher thyroid-stimulating hormone receptor (TSHr) and thyroperoxidase (TPO) protein expression. TPO activity was lower in NIC males. Hydrogen peroxide generation was decreased in NIC males. Activities of superoxide dismutase, catalase and glutathione peroxidase were compromised in NIC animals from both sexes. 4-Hydroxynonenal was higher only in NIC females, while thiol was not affected in NIC animals from both sexes. NIC offspring also had altered expression of sex steroid receptors in thyroid gland. Both sexes showed similar thyroid morphology, with lower follicle and colloid size. Thyroid from female offspring exposed to nicotine during breastfeeding developed oxidative stress, while the male gland seemed to be protected from redox damage. Thyroid dysfunctions seem to be associated with redox imbalance in a sex-dependent manner.

SUBMITTER: Miranda RA

PROVIDER: S-EPMC7519108 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature

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Thyroid redox imbalance in adult Wistar rats that were exposed to nicotine during breastfeeding.

Miranda Rosiane Aparecida RA de Moura Egberto Gaspar EG Soares Patrícia Novaes PN Peixoto Thamara Cherem TC Lopes Bruna Pereira BP de Andrade Cherley Borba Vieira CBV de Oliveira Elaine E Manhães Alex C AC de Faria Caroline Coelho CC Fortunato Rodrigo Soares RS Lisboa Patricia Cristina PC

Scientific reports 20200924 1

Maternal nicotine exposure causes several consequences in offspring phenotype, such as obesity and thyroid dysfunctions. Nicotine exposure can increase oxidative stress levels, which could lead to thyroid dysfunction. However, the mechanism by which nicotine exposure during breastfeeding leads to thyroid gland dysfunction remains elusive. We aimed to investigate the long-term effects of maternal nicotine exposure on redox homeostasis in thyroid gland, besides other essential steps for thyroid ho ...[more]

PMID: 32973319

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Project description:Background:Gastric ulcers are mucosal discontinuities that may extend into the mucosa, submucosa or even deeper. They result from an imbalance between mucosal aggressors and protective mechanisms that include the mucus bicarbonate layer. Thyroid hormones have been shown to accelerate gastric ulcer healing in part by increasing the adherent mucus levels. However, the effects of thyroid hormones on goblet cell numbers and expression of neutral and acidic mucins during ulcer healing have not been investigated. Methods:Thirty six adult male Wistar rats were randomly divided into six groups each with six animals. Group 1 (normal control) and group 2 (negative control) were given normal saline for eight weeks. Groups 3 and 4 were given 100 ?g/kg per day per os of thyroxine so as to induce hyperthyroidism. Groups 5 and 6 received 0.01% (w/v) Propylthiouracil (PTU) for 8 weeks so as to induce hypothyroidism. After thyroid hormonal levels were confirmed using radioimmunoassay and immunoradiometric assays, ulcer induction was done using 40 mg/kg intragastric single dose of Indomethacin in groups 2, 3 and 5. Stomachs were extracted after day 3 and 7 of ulcer induction for histological examination. Histochemistry was carried out using Periodic Acid Shiff and Alcian Blue. The number of acidic and neutral goblet cells were determined by counting numbers per field. Mucin expression (%) was determined using Quick Photo Industrial software version 3.1. Results:The numbers of neutral goblet cells (cells/field) increased significantly (P?<?0.05) in the ulcer+thyroxine (14.67?±?0.33), thyroxine (17.04?±?1.71) and ulcer+PTU (12.89?±?1.06) groups compared to the normal control (10.78?±?1.07) at day 3. For the acidic goblet cells, differences between treatment groups were more pronounced at day 7 between the ulcer+thyroxine (22.56?±?1.26) and thyroxine (22.89?±?0.80). We further showed that percentage expression of both neutral and acidic mucins was significantly higher in the ulcer+thyroxine (9.23?±?0.17 and 6.57?±?0.35 respectively) and thyroxine groups (9.66?±?0.21 and 6.33?±?0.38 respectively) as compared to the normal control group (4.08?±?0.20 and 4.38?±?0.11 respectively) at day 3 after ulcer induction. Conclusion:This study confirms the role played by thyroid hormones in healing of indomethacin induced gastric ulcers. The study further demonstrates increased numbers of both neutral and acidic goblet cells and the increase in expression of both neutral and acidic mucins during healing of indomethacin induced ulcers.

Dataset Information

Thyroid redox imbalance in adult Wistar rats that were exposed to nicotine during breastfeeding.

Publications

Thyroid redox imbalance in adult Wistar rats that were exposed to nicotine during breastfeeding.

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