Biochemical Parameters of Female Wistar Rats and Their Offspring Exposed to Inorganic Mercury in Drinking Water during the Gestational and Lactational Periods.

The aim of this study was to investigate the effects of inorganic mercury (Hg2+) exposure on biochemical parameters of dams and their offspring exposed to metal in drinking water. Female Wistar rats were exposed to 0, 10, and 50 µg Hg2+/mL (as HgCl2) for 42 days corresponding to gestational (21 days) and lactational (21 days) periods. The offspring were sacrificed on postnatal days 10, 20, 30, and 40. Dams exposed to Hg2+ presented a decrease in water intake in gestation [total: F(2,19) = 15.84; p ≤ 0.0001; daily: F(2,21) = 12.71; p = 0.0002] and lactation [total: F(2,19) = 4.619; p = 0.024; daily: F(2,21) = 5.309; p = 0.0136] without alteration in food intake. Dams exposed to 50 µg Hg2+/mL had an increase in kidney total [F(2,21) = 8.081; p = 0.0025] and relative [F(2,21) = 14.11; p = 0.0001] weight without changes in biochemical markers of nephrotoxicity. Moreover, dams had an increase in hepatic [F(2,10) = 3.847; p = 0.0577] and renal [F(2,11) = 6.267; p = 0.0152] metallothionein content concomitantly with an increase in renal Hg levels after Hg2+ exposure. Regarding offspring, the exposure to Hg2+in utero and breast milk increased the relative liver [F(2,18) = 5.33; p = 0.0152] and kidney [F(2,18) = 3.819; p = 0.0415] weight only on the postnatal day 40. In conclusion, dams were able to handle the Hg2+ avoiding the classic Hg2+ toxic effects as well as protecting the offspring. We suggest that this protection is related to the hepatic and renal metallothionein content increase.

Effects of Zinc and N-Acetylcysteine in Damage Caused by Lead Exposure in Young Rats.

This study investigated the toxicity of rats exposed to lead acetate (AcPb) during the second phase of brain development (8-12 days postnatal) in hematological and cerebral parameters. Moreover, the preventive effect of zinc chloride (ZnCl2) and N-acetylcysteine (NAC) was investigated. Pups were injected subcutaneously with saline (0.9% NaCl solution), ZnCl2 (27 mg/kg/day), NAC (5 mg/kg/day) or ZnCl2 plus NAC for 5 days (3rd-7th postnatal days), and with saline (0.9% NaCl solution) or AcPb (7 mg/kg/day) in the five subsequent days (8th-12th postnatal days). Animals were sacrificed 21 days after the last AcPb exposure. Pups exposed to AcPb presented inhibition of blood porphobilinogen-synthase (PBG-synthase) activity without changes in hemoglobin content. ZnCl2 pre-exposure partially prevented PBG-synthase inhibition. Regarding neurotoxicity biomarkers, animals exposed to AcPb presented a decrease in cerebrum acetylcholinesterase (AChE) activity and an increase in Pb accumulation in blood and cerebrum. These changes were prevented by pre-treatment with ZnCl2, NAC, and ZnCl2 plus NAC. AcPb exposure caused no alteration in behavioral tasks. In short, results show that AcPb inhibited the activity of two important enzymatic biomarkers up to 21 days after the end of the exposure. Moreover, ZnCl2 and NAC prevented the alterations induced by AcPb.

Effects of zinc against mercury toxicity in female rats 12 and 48 hours after HgCl2 exposure.

This work investigated the toxicity of inorganic mercury and zinc preventive effects in female rats sacrificed 12 or 48 h after HgCl2 exposure. Female Wistar rats were subcutaneously injected with ZnCl2 (27 mg/kg) or saline (0.9 %), and 24 h later they were exposed to HgCl2 (5 mg/kg) or saline (0.9 %). Rats sacrificed 12 hours after Hg administration presented an increase in kidney weight and a decrease in renal ascorbic acid levels. Zinc pretreatment prevented the renal weight increase. Rats sacrificed 48 h after Hg exposure presented a decrease in body weight gain, an increase in renal weight, a decrease in renal δ-aminolevulinic acid dehydratase activity, an increase in serum creatinine and urea levels, and a decrease in kidney total thiol levels. Zinc pretreatment partly prevented the decrease in body weight gain and increase in creatinine levels, in addition to totally preventing renal δ-aminolevulinic acid dehydratase inhibition. Mercury accumulation in the kidney and liver in both periods was observed after Hg administration. These results show the different Hg effects along the time of intoxication, and a considerably preventive effect of zinc against Hg toxicity.

Inorganic mercury exposure in drinking water alters essential metal homeostasis in pregnant rats without altering rat pup behavior.

The aim of this work was to investigate the effects of HgCl2 exposure in the doses of 0, 10 and 50µg Hg2+/mL in drinking water during pregnancy on tissue essential metal homeostasis, as well as the effects of HgCl2 exposure in utero and breast milk on behavioral tasks. Pregnant rats exposed to both inorganic mercury doses presented high renal Hg content and an increase in renal Cu and hepatic Zn levels. Mercury exposure increased fecal Hg and essential metal contents. Pups exposed to inorganic Hg presented no alterations in essential metal homeostasis or in behavioral task markers of motor function. In conclusion, this work showed that the physiologic pregnancy and lactation states protected the offspring from adverse effects of low doses of Hg2+. This protection is likely to be related to the endogenous scavenger molecule, metallothionein, which may form an inert complex with Hg2+.