Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q7LGC8 (HSD)
 3,196 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic, low-level exposures to environmental toxicants, because they often begin prenatally and then persist throughout the individual's lifetime, pose challenging issues to risk assessment. Exposure to low levels of methylmercury through the diet, based largely on consumption of fish and sea mammals, follows this pattern. Early development is considered to be a period of heightened vulnerability during which even low-level exposures may produce undetected, "silent", damage that is revealed only under conditions that challenge the functional capacities of the individual. Aging, with its diminished functional capacities and compensatory reserves provides such a challenge, but, to explore this possibility, requires basic information about blood and brain levels under conditions of chronic lifetime exposure. The current research was undertaken to provide such information. One hundred female B6C3F1/HSD mice were assigned to one of three dose groups, 0, 1, or 3 ppm methylmercury chloride administered in a 5 nM sodium carbonate drinking solution. They were bred with male CBA/J HSD mice to produce the trihybrid offspring B6C3F1/ HSD x CBA/J HSD. Dosing of the females began 4 weeks prior to breeding and continued for the two methylmercury-exposed groups throughout breeding and gestation. The methylmercury-treated litters were split into two subgroups, one exposed throughout its lifetime (set at 26 months) to the original dose, the other exposed through postnatal day 13 (PND 13). Brain and blood concentrations were assayed by cold-vapor atomic absorption. Samples were obtained on PND 4 and 21, and then at the end of months 14 and 26. On PND 4, brain and blood levels closely reflected maternal dosing. In all groups, concentrations fell sharply from PND 4 to 21, but to a greater extent in the perinatal groups. Blood levels in the 1 ppm lifetime group remained unchanged between months 14 and 26, but brain levels rose modestly. In the 3 ppm lifetime group, both brain and blood levels rose significantly between months 14 and 26, suggesting an interaction between dose and age.
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PMID:Perinatal and lifetime exposure to methylmercury in the mouse: blood and brain concentrations of mercury to 26 months of age. 1157 26

The effect of colloidal solutions on bacterial translocation was studied. Sublethal hemorrhagic shock was established by blood withdrawal until the mean arterial pressure fell to 40 mmHg within 15 min on 36 adult Wistar Albino rats. Resuscitation was performed using four different solutions with the same amount of blood. Group I (n = 9) 0.9% NaCl, Group II (n = 9) 10% dextran 40, Group III (n = 9) 6% hydroxyethyl starch, Group IV (n = 9) 4% modified fluid gelatin. Before resuscitation and after anesthesia blood samples were drawn to analyze pH, PCO2, PO2, SaO2, HCO3 and ABE values. Twenty-four hours after anesthesia laparotomy was performed to obtain tissue samples of the liver, spleen and mesenteric lymph nodes. Samples were cultured on EMB and blood agar media. Results were analyzed with the one-way ANOVA and Post-hoc test (Tukey's HSD). The translocated bacteria were mainly Eschericia coli and three grew in Group I, two in Group II, three in Group III and six in Group IV. Although there was a trend in difference in bacterial translocation rates among groups, statistical analyses revealed no difference among groups (p < 0.05). It can be concluded that resuscitation with modified gelatin causes higher bacterial translocation in an experimental sublethal hemorrhagic shock model.
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PMID:Resuscitation with modified gelatin causes higher bacterial translocation in experimental sublethal hemorrhagic shock. 1549 Oct 72

This project was undertaken to more completely understand the consequences of lifetime exposure to methylmercury. A series of experiments examined how perinatal or lifetime exposure to methylmercury affected behavioral performances in the adult mouse at different ages. One hundred female B6C3F1/HSD mice were assigned to one of three dose groups, 0 ppm, 1 ppm, or 3 ppm methylmercury chloride administered in a 5 nM sodium carbonate drinking solution. Four weeks after initiating dosing, the females were bred with male CBA/J HSD mice to produce the trihybrid offspring B6C3F1/HSD x CBA/J HSD. The methylmercury-treated litters were split into two subgroups, one exposed throughout its lifetime to the original dose, the other exposed through postnatal day 13. Altogether, then, five groups were studied: Control, 1 ppm perinatal, 1 ppm lifetime, 3 ppm perinatal, and 3 ppm lifetime. Three neurobehavioral indices were evaluated: (1) delayed spatial alternation (a test of memory) and (2) running in a wheel to earn food pellets (schedule-controlled operant behavior) were assessed starting at 5 and 15 months of age; (3) hindlimb splay, a measure of motor function, was assessed at 5, 15, and 26 months of age. Subjects tested at one age were littermates of those tested at the other ages. MeHg altered the hindlimb splay distance; control mice differed from methylmercury-exposed mice, the 1 ppm lifetime and 3 ppm lifetime groups differed from each other, and the analysis yielded an age by dose interaction. MeHg exposure altered different measures of wheel running under the 3 ppm lifetime condition. In the delayed alternation procedure, the mouse was required to respond to one of two locations in a strictly alternating sequence. More mice from the treated groups, except for the 1 ppm perinatal group, failed to meet the criterion at longer delay values. Overall, the results show that exposure to low levels of methylmercury produces behavioral effects that depend on the test procedure, the dose, the duration of exposure, and the age. Lifetime evaluations of exposure to toxicants, beginning with early development, should be a component of the risk assessment process for neurotoxicity.
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PMID:Perinatal and lifetime exposure to methylmercury in the mouse: behavioral effects. 1597 Mar 29