Nickel chloride (NiCl₂) is a heavy metal that may affect the function of the thyroid. Selenium (Se) and zinc (Zn) are essential trace elements involved in thyroid hormone metabolism. However, little is reported about thyrotoxicity during gestation. The current study aimed to investigate the protective effects of selenium and zinc against NiCl₂-induced thyrotoxicity in pregnant Wistar rats. Female rats were treated subcutaneously (s.c.) on the 3rd day of pregnancy, with NaCl 0.9% and served as control, NiCl₂ (100 mg/kg body weight (BW)) alone, or in association with Se (0.3 mg/kg, s.c.), ZnCl₂ (20 mg/kg, s.c.), or both of them simultaneously. Oxidative stress parameters, thyroid biomarkers, and histopathological examination were evaluated. Results showed that NiCl₂ exposure caused a significant decrease in maternal body weight and an increase in absolute and relative thyroid weight compared to the controls. NiCl₂ administration also led to decreased plasma triiodothyronine (T3) and thyroxine (T4) with a concomitant significant increase in thyroid-stimulating hormone (TSH) levels when compared to that of control. In addition, an overall pro-oxidant effect was associated with a decrease in the reduced glutathione (GSH) and nonprotein thiol (NPSH) contents and the enzymatic activity of glutathione peroxidase (GPx) and superoxide dismutase (SOD), and an increase in malondialdehyde (MDA). These biochemical disturbances were confirmed by histological changes. However, the co-treatment of Se and/or ZnCl₂ attenuates NiCl₂-induced changes. Our findings suggested that Se and ZnCl₂ ameliorated NiCl₂-induced thyrotoxicity in pregnant Wistar rats by exhibiting antioxidant effects.

Hexavalent chromium (CrVI) compounds are potent toxicants commonly used in numerous industries. Thus, potential toxic effects and health hazards are of high relevance. Selenium (Se) and zinc (Zn) are known for their antioxidant and chemoprotective properties. However, little is known about their protective effects against CrVI-induced renal damage during pregnancy. In this context, the present study aimed to investigate the protective efficacy of these two essential elements against potassium dichromate-induced nephrotoxicity in pregnant Wistar Albino rats. Female rats were divided into control and four treated groups of six each receiving subcutaneously on the 3rd day of pregnancy, K₂Cr₂O₇ (10 mg/kg, s.c. single dose) alone, or in association with Se (0.3 mg/kg, s.c. single dose), ZnCl₂ (20 mg/kg, s.c. single dose) or both of them simultaneously. The nephrotoxic effects were monitored by the evaluation of plasma renal parameters, oxidative stress biomarkers, DNA damage, and renal Cr content. The obtained results showed that K₂Cr₂O₇ disturbed renal biochemical markers, induced oxidative stress and DNA fragmentation in kidney tissues, and altered renal histoarchitecture. The co-administration of Se and/or ZnCl₂ has exhibited pronounced chelative, antioxidant, and genoprotective effects against K₂Cr₂O₇-induced renal damage and attenuated partially the histopathological alterations. These results suggest that Se and Zn can be used as efficient nephroprotective agents against K₂Cr₂O₇-induced toxicity in pregnant Wistar Albino rats.

Hexavalent chromium (CrVI) is an environmental pollutant and an endocrine-disrupting metal. Se and Zn are essential trace elements, known to play a crucial role in thyroid homeostasis. However, there is a lack of data reporting thyrotoxicity during gestation. In this study, we investigated the protective effects of selenium and zinc against potassium dichromate–induced thyrotoxicity in pregnant Wistar rats. Thirty pregnant Wistar rats were divided into control and four treated groups receiving subcutaneously (s.c) on the 3rd day of pregnancy, K₂Cr₂O₇ (10 mg/kg, s.c) alone, or in association with Se (0.3 mg/kg, s.c), ZnCl₂ (20 mg/kg, s.c), or both of them simultaneously. The hormonal profile, oxidative stress biomarkers, DNA damage, and histological modifications were evaluated. Our main findings showed that K₂Cr₂O₇ promoted hypothyroidism, oxidative stress, genotoxicity, and histological alterations in the thyroid gland. The co-treatment with Se or ZnCl₂ has mitigated K₂Cr₂O₇-induced thyrotoxicity in pregnant Wistar rats by exhibiting antioxidant and genoprotective effects. However, the combined co-treatment of both of them was less thyroprotective, and therefore, further investigations on the synergetic interaction of Se and Zn against CrVI toxicity using different doses and exposure routes are required.

Nickel chloride (NiCl₂) is a heavy metal that may affect the function of the thyroid. Selenium (Se) and zinc (Zn) are essential trace elements involved in thyroid hormone metabolism. However, little is reported about thyrotoxicity during gestation. The current study aimed to investigate the protective effects of selenium and zinc against NiCl₂-induced thyrotoxicity in pregnant Wistar rats. Female rats were treated subcutaneously (s.c.) on the 3rd day of pregnancy, with NaCl 0.9% and served as control, NiCl₂ (100 mg/kg body weight (BW)) alone, or in association with Se (0.3 mg/kg, s.c.), ZnCl₂ (20 mg/kg, s.c.), or both of them simultaneously. Oxidative stress parameters, thyroid biomarkers, and histopathological examination were evaluated. Results showed that NiCl₂ exposure caused a significant decrease in maternal body weight and an increase in absolute and relative thyroid weight compared to the controls. NiCl₂ administration also led to decreased plasma triiodothyronine (T3) and thyroxine (T4) with a concomitant significant increase in thyroid-stimulating hormone (TSH) levels when compared to that of control. In addition, an overall pro-oxidant effect was associated with a decrease in the reduced glutathione (GSH) and nonprotein thiol (NPSH) contents and the enzymatic activity of glutathione peroxidase (GPx) and superoxide dismutase (SOD), and an increase in malondialdehyde (MDA). These biochemical disturbances were confirmed by histological changes. However, the co-treatment of Se and/or ZnCl₂ attenuates NiCl₂-induced changes. Our findings suggested that Se and ZnCl₂ ameliorated NiCl₂-induced thyrotoxicity in pregnant Wistar rats by exhibiting antioxidant effects.

Nickel Is A Heavy Metal That May Affect The Function Of The Thyroid. The Present Study Was Undertaken To Assess The Protective Effects Of Selenium And Zinc Against Nickel-induced Thyrotoxicity In Preimplanted Wistar Albino Rats. Nickel Is Administered Alone (100 Mg/kg Body Weight) Subcutaneously Or In Combination With Selenium (0.3 Mg/kg Body Weight) Either With Zinc (20 Mg/kg Body Weight) Or Combined With Both Selenium And Zinc. All Groups Of Rats Were Injected On Day 3 Of Gestation In The Pre-implantation Period. Exposure Of Rats To Nickel Caused A Significant Decrease In Maternal Body Weight On Days 6 And 20 Of Gestation And An Increase In Absolute And Relative Thyroid Weight Compared To The Controls. Nickel Treatment Was Also Led In Decreased Plasma Triiodothyronine, Thyroxine With A Concomitant Significant Increase In Thyroid-stimulating Hormone Levels When Compared To Control. These Changes Were Confirmed By Histological Damages. However, Co-administration Of Selenium And/or Zinc To Nickel-treated Rats Restored The Hormonal And Histological Aspects. Our Findings Suggested That Selenium And Zinc Ameliorated Nickel Induced Thyroid Damage.

: The aim of this study was to investigate that nickel chloride (NiCl2) induced reproductive toxicity in pre- implanted Wistar Rats and examined the possible protective effect of zinc chloride and selenium on plasma concentration of the hormones of 17 b etradiol (E2) and progesterone (prog); on the reproductive organ’s histology and on development. Experimental results showed the subcutaneous (s.c) administration of Nicl2 to Wistar albino Rats induced a decrease in plasma concentration of E2 and prog in addition, disturbance in development parameters and structural damages to the histology of the reproductive organs. Conversely, Se and ZnCl2 dues to the antioxidants property, regulate the secretion of E2 and Prog hormones, prevent alterations in the reproductive organs and in development in preimplanted rates receiving NiCl2.