Experimental leptospirosis: Leptospira canicola infection in calves.
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Agglutination Tests↗
Biomedical subjects
S D Sleight
Publications and source records attributed to S D Sleight.
Lesions of infectious arthritis in calves.
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Animals↗
Leptospira pomona in tissue culture: preliminary study.
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Acid-Base Equilibrium↗
Toxicity and microsomal enzyme induction effects of several polybrominated biphenyls of Firemaster.
Some toxicological and pharmacological effects of 2,4,5,2',5'-penta- (congener 1), 2,3,4,2',4',5'-hexa- (congener 5), 2,4,5,3',4',5'-hexa- (congener 6), 2,3,4,5,3',4',-hexa- (congener 7), and 2,3,4,5,2',3',4'-heptabromobiphenyl (congener 9) were evaluated in male rats given a single 90 mg/kg ip injection and killed seven days later. Only congener 7 depressed body weight gain, spleen and thymus weights, and caused severe histopathological changes in the thymus. Congener 7 caused the largest increase in liver weight and the most changes in liver pathology while congener 1 failed to enlarge this organ and caused the mildest ultrastructural changes. Liver microsomes were isolated and evaluated for enzyme induction from all treated rats except those administered congener 6, which was previously identified as a mixed-type enzyme inducer (Dannan et al., 1978b). All congeners increased the liver microsomal cytochrome P-450 content, but only congener 7 shifted the carbon monoxide difference spectrum absorption maximum to 448.0 nm. The microsomal ethyl isocyanide difference spectrum 455/430 nm ratio was increased the most by congener 7 (3 fold). All congeners increased cytochrome P-450 reductase and microsomal epoxide hydrase activities by nearly 1.5-3 fold. Congener 7 failed to induce aminopyrine-N-demethylase activity but the remaining congeners increased it by 2 fold. Congener 7 was the most effective inducer of benzo[a]pyrene hydroxylase and p-nitrophenol UDP-glucuronyl transferase. These results add to the suggestion that the presence of an ortho halogen on a polyhalogenated biphenyl does not completely abolish toxicity or 3-methylcholanthrene-type microsomal enzyme induction.
Animals↗
Renal protein degradation: a biochemical target of specific nephrotoxicants.
Protein degradation in the kidney occurs mainly in lysosomes, organelles which may also accumulate nephrotoxic chemicals. The goal of this study was to evaluate the effects of intracellular accumulation of gentamicin, cephaloridine and cisplatin on lysosomal digestion of the protein lysozyme. Gentamicin (15 or 30 mg/kg/day for 3 or 5 days), cisplatin (2.5 or 5 mg/kg) or cephaloridine (500, 1000, 2000 or 2500 mg/kg) was administered ip to male Wistar rats. The main site of the nephrotoxic effects of these compounds was the proximal tubule where these agents differentially affected S1, S2 and/or S3 segments. A 2- and 4-fold increase of the excretion of N-acetyl-beta-D-glucosaminidase (NAG) was observed in the urine from cisplatin- and gentamicin-treated rats, respectively; no change in enzyme excretion occurred after cephaloradine. One hour prior to sacrifice, rat were given 0.3 mg of unlabelled lysozyme in combination with 125I-lysozyme in 0.3 mL saline. Renal cortical slices were prepared and incubated for 15, 30, 60 and 90 min. Release of trichloroacetic acid (TCA) soluble radioactivity into the medium was assumed to quantify lysosomal degradation of lysozyme. Accumulation of p-amino-hippurate (PAH) in renal cortical slices and changes in blood urea nitrogen (BUN) concentration were used as indices of renal damage. TCA-soluble radioactivity increased in the medium from kidney slices from control rats to 50% of the total radioactivity after 90 min incubation. In gentamicin-treated rats, lysozyme degradation was significantly decreased by doses of 15 and 30 mg/kg/day after 3 and 5 days of exposure in the absence of any changes in BUN or PAH accumulation.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Insensitivity of the chicken embryo to the ototoxicity of aminoglycoside antibiotics and a loop diuretic.
Guinea pigs are routinely used in the histological evaluation of the cochlea as a method of testing for ototoxicity, but the procedures are very time-consuming. Because the avian cochlea is easier to examine and newly hatched chicks are sensitive to the ototoxic effects of gentamicin, birds may be useful in testing for ototoxicity. The use of chicken embryos would be even better for testing, but whether or not chicken embryos are sensitive to ototoxicants is unknown. In an attempt to determine whether or not chicken embryos may be used instead of guinea pigs in screening tests for ototoxicity, aminoglycoside antibiotics and a loop diuretic, ethacrynic acid, were administered to chicken embryos. A maximum-tolerated dose of gentamicin, kanamycin, streptomycin, ethacrynic acid, or a combination of gentamicin and ethacrynic acid was administered to fertile eggs of White Leghorn chickens on incubation days 10-17. To compare the effect of route of exposure on ototoxicity, gentamicin was administered by injection into the allantoic space, yolk sac, and air cell as well as by submerging the egg in gentamicin solution. With the preferred air cell route the effects of the ototoxic drugs kanamycin, streptomycin, ethacrynic acid, and a combination of ethacrynic acid and gentamicin were compared. On incubation day 18, cochleas were removed from the chicken embryos. Serial sections of these avian cochleas were examined and hair cells were counted. No significant difference was seen between the number of hair cells in cochleas of control chicken embryos and those from chicken embryos treated with drugs. Therefore, the chicken embryo appears to be insensitive to the ototoxicity of aminoglycoside antibiotics and a loop diuretic.
Animals↗
Distribution of gentamicin to the cochlea of the chicken embryo.
Aminoglycoside antibiotics are ototoxic in mammals and birds, including recently hatched chicks, but chicken embryos are insensitive to the ototoxicity of gentamicin, kanamycin, and streptomycin. To determine whether or not the insensitivity is due to a lack of antibiotic distribution to the avian cochlea, the distribution of gentamicin to the cochlea of the White Leghorn chicken embryo was compared to the distribution to the cochlea of the recently hatched White Leghorn chick. Fertile eggs were injected with a maximally tolerated dose of gentamicin sulfate (0.1 mg/egg/day) on incubation days 10-18, and the chicks were injected subcutaneously with either 5 mg (non-ototoxic) or 100 mg (ototoxic) gentamicin sulfate/kg body weight on days 1-9 after hatching. Gentamicin sulfate was histochemically detected within the basilar papilla (the avian equivalent of the organ of Corti) in all treated chicken embryos and chicks by 1 day after the first injection, and the staining was intense after 3 days of treatment. By ultrastructural immunocytochemistry, mild, diffuse labeling for gentamicin sulfate was detected within the endoplasmic reticulum of short and tall hair cells of chicken embryos by incubation day 17. Moderate labeling of gentamicin sulfate was detected in the infracuticular region of lysosomes of hair cells in chicks receiving 5 treatments of gentamicin sulfate at 5.0 mg/kg body weight and after 1 treatment of gentamicin sulfate at 100 mg/kg body weight.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Tumor-promoting effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin and phenobarbital in initiated weanling Sprague-Dawley rats: a quantitative, phenotypic, and ras p21 protein study.
In an initiation-promotion protocol, female weanling Sprague-Dawley rats were initiated with 10 mg/kg nitrosodiethylamine and promotion was started after 30 days. Promotion regimens were as follows: 2,3,7,8-tetrachlorodibenzo-para-dioxin (TCDD; 150 ppt in diet) continuously until day 450; phenobarbital (PB; 500 ppm in diet) until day 170; PB until day 170, followed by TCDD until day 240; and PB until day 170, followed by a basal diet (BD) until day 240 and subsequently TCDD from days 240 to 450. TCDD fed to initiated rats had a promoting effect on the development of adenosine triphosphatase-negative altered hepatocellular foci (AHF). At 450 days, the volume fraction of liver occupied by AHF was increased in initiated rats given TCDD continuously and in those given PB followed by TCDD, whereas the mean volume of AHF was significantly larger in initiated rats given TCDD continuously. PB and TCDD promoted similar phenotypes of AHF as seen in hemotoxylin and eosin-stained sections, but the eosinophilic phenotype most closely correlated with the development of hepatocellular neoplasms. The protooncogene product ras p21 protein was present in the majority of PB- and TCDD-promoted AHF, hepatocellular adenomas, and hepatocellular carcinomas. Eosinophilic AHF and ras p21 protein expression most closely correlated with neoplastic development, suggesting that these cell populations, when promoted, may be at greater risks for developing into neoplasms.
Animals↗
Biological and induction effects of phenobarbital and 3-methylcholanthrene in mink (Mustela vison).
Mink were injected (ip) daily with 20 mg/kg of 3-methylcholanthrene (MC) or 40 mg/kg of phenobarbital (PB) for 3 days and killed 48 hr after the last injection. The duration of anesthetic action of PB increased after each injection. MC-treated mink became anorexic and lost substantial body weight. PB caused enlargement of liver and lungs, whereas MC caused liver atrophy. No major treatment-related morphologic changes including amount of endoplasmic reticulum (ER) in liver were revealed by electron microscopic examination. Microsomal protein content was not increased and NADPH cytochrome P-450 reductase was not induced in liver by either PB or MC. Cytochrome P-450 (448) was increased 3.2-fold by PB and 2.5-fold by MC. Cytochrome b5 was increased 2.3-fold by MC but was not affected by PB. Aminopyrine N-demethylase was enhanced 5.1-fold in activity by PB whereas hexobarbital hydroxylase was not induced. MC-treatment moderately increased the activities of benzo(a)pyrene hydroxylase (1.7-fold) and ethoxyresorufin O-deethylase (2.1-fold) but had no effect on ethoxycoumarin O-deethylase. The most distinctive features of the mink revealed by this study are a) lack of PB induction of the ER, microsomal protein content, NADPH-cytochrome P-450 reductase, and hexobarbital hydroxylase, and b) lack of MC induction of cytochrome P-448-associated mixed function oxidases that are known to be highly responsive to MC in other species.
Animals↗
Pathologic effects of 2,2',4,4',5,5'-and 2,3',4,4',5,5'-hexabromobiphenyl in white leghorn cockerels.
Pathologic effects of 2,2',4,4',5,5'-hexabromobiphenyl (HBB), 2,3',4,4',5,5'-HBB, and a commercial mixture of polybrominated biphenyls (PBB) were compared in White leghorn cockerels. Diets containing 1, 10, or 100 ppm PBB, 4 or 10 ppm 2,3',4'4',5,5'-HBB, or 10 or 62 ppm 2,2',4,4',5,5'-HBB were fed for 28 days. Doses of 10 ppm of each chemical were used to provide a direct comparison of toxicity. Since nearly 4% of PBB consists of 2,3',4,4',5,5'-HBB and approximately 62% consists of 2,2',4,4',5,5'-HBB, effects of doses of 4 and 62 ppm, respectively, were compared with effects of 100 ppm of PBB to determine if either of the congeners were mainly responsible for the pathologic effects caused by the mixture. Liver weights were increased in cockerels fed diets containing 62 ppm of 2,2',4,4',5,5'-HBB or 10 or 100 ppm PBB. Hepatocytes were enlarged and vacuolated and lymphoid cells of the bursa of Fabricius were depleted by 10 ppm 2,3',4,4',5,5'-HBB, ppm 2,2',4,4',5,5'-HBB, and 10 or 100 ppm PBB. These dietary concentrations caused ultrastructural changes in hepatocytes consisting of vacuolation, increased smooth endoplasmic reticulum, swollen mitochondria, and disruption of mitochondrial cristae. When either of the congeners were given in concentrations relative to their concentrations in PBB, they were less toxic than the mixture. When concentrations in diets were equal, PBB caused more severe effects than 2,3',4,4',5,5'-HBB. The least effects were seen with 2,2',4,4',5,5'-HBB. Results indicate that the two congeners chosen for study are not individually as toxic as the parent mixture.
Animals↗