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.

-Objective: Potassium dichromate (K 2 Cr 2 O 7 ) is a potent pollutant for human and animal health. The purpose of the current work is to compare the effect of K 2 Cr 2 O 7 using variations in the dose, route of administration and duration of exposure in male and female Wistar albino rats and to research the interaction of chromium and selenium with a special focus on hematopoiesis. Materials and methods: K 2 Cr 2 O 7 was subcutaneously administered alone (10, 50 and 100 mg/kg body weight) or K 2 Cr 2 O 7 (10 mg/kg) in association with selenium (0.3 mg/kg) was administered to female Wistar albino rats. Male rats received in their drinking water K 2 Cr 2 O 7 (30 mg/L/day) alone or in association with Se (0.3 mg/L/day) for 20 consecutive days. The hematological parameters were evaluated on days 3, 6 and 21 after subcutaneous (sc.) treatment in female rats and on days 10 and 20 after oral administration in male rats. Results: K 2 Cr 2 O 7− induced during the first three days a significant (p < 0.05) dose-dependent decrease in the number of erythrocytes, platelets, leucocytes, lymphocytes and the hematocrit levels, and a dose-dependent increase in the number of granulocytes and monocytes. In the drinking water, chromium sc. significantly decreased the number of leucocytes and lymphocytes on day 10 after treatment and elevated the number of granulocytes and monocytes 20 days later. Selenium sc. counterbalanced the hematotoxic effects of chromium in female rats. Conclusion: These results suggest that the selenium has a protective role against the hematotoxicity of subcutaneous chromium in female Wistar rats.Key words: Chromium, rat, selenium, hematotoxicity Résumé -Objectif : Le dichromate de potassium (K 2 Cr 2 O 7 ) est un polluant potentiellement néfaste pour la santé humaine et animale. Cette étude a été entreprise afin de rechercher une éventuelle interaction entre le K 2 Cr 2 O 7 et le sélénium (Se) sur l'hématopoïèse chez les rats albinos Wistar mâles et femelles. Matériel et Méthodes : Le K 2 Cr 2 O 7 est administré seul (10, 50 et 100 mg/kg) par voie sous-cutanée (sc) ou en association (10 mg/kg) avec le sélénium (0,3 mg/kg). Les rats mâles reçoivent dans l'eau de boisson le K 2 Cr 2 O 7 (30 mg/L/jour) seul ou en association avec le sélénium (0,3 mg/L/jour) pendant 20 jours consécutifs. Les variations des paramètres hématologiques sont évaluées au 3 e , 6 e et 21 e jour chez les rattes et au 10 e et 20 e jour chez les mâles. Résultats : Les résultats montrent que le chrome engendre dès le 3 e jour après son administration par voie sc chez la femelle une diminution notable et dose-dépendante (p < 0,05) du nombre d'érythrocytes, du taux d'hématocrite, du nombre de plaquettes sanguines, de leucocytes, de lymphocytes et une augmentation dose-dépendante du nombre de granulocytes et de monocytes. Le chrome administré par voie orale diminue le nombre de leucocytes et de lymphocytes dès le 10 e jour du traitement et augmente celui des monocytes et des granulocytes 20 jours plus tard. La présence du sélénium ...

The effects of two enkephalinase inhibitors, acetorphan and thiorphan, and the enkephalin analogue [D-Ala2-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-1) and thiorphan (1 mg kg-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 mumol l-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 micrograms per 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-1 s.c.) increased both the amplitude and duration of uterine motility in vivo; however, naloxone (26 mumol l-1 and 52 mumol l-1) produced a paradoxical dose-dependent biphasic effect in vitro.

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