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.

The exposure to nickel chloride (NiCl₂) can cause hematotoxicity and hepatotoxicity and canaffect development. The present study pertains to the protective effect of selenium (Se) against NiCl₂-induced toxicity in preimplanted Wistar albino rats. The subcutaneous (s.c.) administration of 25 or 50 mg/kg of NiCl₂ to Wistar albino rats on day 3 of gestation induced an immediate and significant decrease in maternal body weight and anemia 2 days after treatment. In addition, an increase in plasma aspartate aminotransferase (AST) was observed. These effects were maintained on day 20 of gestation. Moreover, a significant increase in plasma alanine aminotransferase (ALT) levels was observed with the administration of 25 mg/kg of NiCl₂. Conversely, administration of 50 mg/kg of NiCl₂ by s.c. injection increased erythropoiesis at day 20 of gestation and decreased platelets counts. In addition, administration of 100 mg/kg of NiCl₂ markedly reduced the maternal body weight and number of live fetuses and increased fetal loss, predominantly at the end of the experimental period. All dose levels of NiCl₂ caused an alteration in the hepatic histoarchitecture. When 0.3-mg/kg Se was injected s.c. with 100-mg/kg NiCl₂, the levels of plasma AST and ALT and the structure of the liver were restored. Administration of 20 mg/L/day of NiCl₂ in the drinking water significantly reduced the maternal body weight at day five of gestation as well as erythropoiesis during the exposure period. The present study suggests that Se can counteract the nocuous effect of nickel on the liver; however this antioxidant did not prevent alterations in development and erythropoiesis. © 2011 Wiley Periodicals, Inc. Environ Toxicol 2013.

The effects of two enkephalinase inhibitors, acetorphan and thiorphan, and the enkephalin analogue [d-Ala²\p=n-\Met⁵]-enkephalinamide (DAMEA), on spontaneous uterine contractions were studied at day 21 of pregnancy in rats following treatment in vivo or in vitro. Acetorphan (10 mg kg\m=-\1)and thiorphan (1 mg kg\m=-\1),immediately after their i.v. administration, increased the duration of spontaneous contractions 3.4- and 4.6-fold, respectively, but did not modify the maximum amplitude. Similarly, thiorphan (40 \g=m\moll\m=-\1) increased the duration of contractions when administered in vitro. Thiorphan was ineffective during the first 30 min when given into the cerebral ventricles (50 \g=m\gper rat). These results suggest that the enkephalinase inhibitors are acting via a peripheral opioid pathway; and this conclusion is supported by the observation that thiorphan potentiated the stimulatory effect of a submaximal dose of DAMEA administered in vitro. The excitatory effects of DAMEA and the enkephalinase inhibitors were blocked by naloxone. This antagonistic effect of naloxone on uterine motility in the periparturient rat uterus, induced by either acetorphan and thiorphan or DAMEA, seems to be regulated by peripheral opiate receptors. Naloxone (10 mg kg\m=-\1 s.c.) increased both the amplitude and duration of uterine motility in vivo; however, naloxone (26 \g=m\moll\m=-\1 and 52 \g=m\moll\m=-\1) produced a paradoxical dose-dependent biphasic effect in vitro.