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+.

Lactating and nonlactating rats differ to renal toxicity induced by mercuric chloride: the preventive effect of zinc chloride.

This study evaluated the effects of HgCl2 on renal parameters in nonlactating and lactating rats and their pups, as well as the preventive role of ZnCl2 . Rats received 27 mg kg(-1) ZnCl2 for five consecutive days and 5 mg kg(-1) HgCl2 for five subsequent days (s.c.). A decrease in δ-aminolevulinic acid dehydratase (δ-ALA-D) activity in the blood and an increase in urine protein content in renal weight as well as in blood and urine Hg levels were observed in lactating and nonlactating rats from Sal-Hg and Zn-Hg groups. ZnCl2 prevented partially the δ-ALA-D inhibition and the proteinuria in nonlactating rats. Renal Hg levels were increased in all HgCl2 groups, and the ZnCl2 exposure potentiated this effect in lactating rats. Nonlactating rats exposed to HgCl2 exhibited an increase in plasma urea and creatinine levels, δ-ALA-D activity inhibition and histopathological alterations (necrosis, atrophic tubules and collagen deposition) in the kidneys. ZnCl2 exposure prevented the biochemical alterations. Hg-exposed pups showed lower body and renal weight and an increase in the renal Hg levels. In conclusion, mercury-induced nephrotoxicity differs considerably between lactating and nonlactating rats. Moreover, prior exposure with ZnCl2 may provide protection to individuals who get exposed to mercury occupationally or accidentally.

Biochemical parameters of pregnant rats and their offspring exposed to different doses of inorganic mercury in drinking water.

This work investigated the effects of low and high doses of inorganic mercury in drinking water on biochemical parameters of pregnant rats and their offspring. Female Wistar rats were treated during pregnancy with 0, 0.2, 0.5, 10 or 50 µg Hg(2+)/mL as HgCl(2). Rats were euthanized on day 20 of pregnancy. Pregnant rats presented a decrease in total water intake in all doses of mercury tested. At high doses, a decrease in the total food intake and in body weight gain was observed. Pregnant rats exposed to 50 µg Hg(2+)/mL presented an increase in kidney relative weight. Mercury exposure did not change serum urea and creatinine levels in any of the doses tested. Moreover, mercury exposure did not change porphobilinogen synthase activity of kidney, liver and placenta from pregnant rats in any of the doses tested, whereas fetuses of pregnant rats exposed to 50 µg Hg(2+)/mL presented an increase in the hepatic porphobilinogen synthase activity. In general, pregnant rats presented alterations due to HgCl(2) exposure in drinking water. However, only the dose 50 µg Hg(2+)/mL appeared to be enough to cross the blood-placenta barrier, since at this dose the fetuses presented change in the porphobilinogen synthase activity.

Delta-aminolevulinate dehydratase activity in red blood cells of rats infected with Trypanosoma evansi.

The aim of this study was to evaluate the activity of delta-aminolevulinate dehydratase (δ-ALA-D) in red blood cells of rats infected with Trypanosoma evansi and establish its association with haematocrit, serum levels of iron and zinc and lipid peroxidation. Thirty-six male rats (Wistar) were divided into 2 groups with 18 animals each. Group A was non-infected while Group B was intraperitoneally infected, receiving 7·5×106 trypomastigotes per animal. Each group was divided into 3 subgroups of 6 rats and blood was collected during different periods post-infection (p.i.) as follows: day 5 (A1 and B1), day 15 (A2 and B2) and day 30 PI (A3 and B3). Blood samples were collected by cardiac puncture to estimate red blood cell parameters (RBC), δ-ALA-D activity and serum levels of iron, zinc and thiobarbituric acid reactive substances (TBARS). Rats in group B showed a significant (P<0·05) reduction of RBC count, haemoglobin concentration and haematocrit at days 5 and 15 p.i. The activity of δ-ALA-D in blood was significantly (P<0·001) increased at days 15 and 30 p.i. δ-ALA-D activity in blood had a significant (P<0·05) negative correlation with haematocrit (r=-0·61) and haemoglobin (r=-0·70) at day 15 p.i. There was a significant (P<0·05) decrease in serum iron and zinc levels and an increase in TBARS levels (P<0·05) during infection. The δ-ALA-D activity in blood was negatively correlated with the levels of iron (r=-0·68) and zinc (r=-0·57) on day 30 p.i. It was concluded that the increased activity of δ-ALA-D in blood might have occurred in response to the anaemia in remission as heme synthesis was enhanced.