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Male Sprague-Dawley rats were pretreated i.p. with corn oil or DMSO (1.5 ml/kg/day), or with beta-naphthoflavone (BNF, 40 mg/kg/day) in corn oil or DMSO for 3 days. 1-Nitropyrene (1-NP, 150 mg/kg) in DMSO was injected i.p. 24 hr after pretreatment. A significant increase in the levels of several serum enzymes was seen in rats pretreated with corn oil alone 24 hr after 1-NP injection. The increase in enzyme activities was significantly reduced by a 3-day pretreatment with DMSO or BNF.

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Male Sprague-Dawley rats were treated with a single i.p. injection of DMSO (3.0 ml/kg) or 9-nitrophenanthrene (9-NP, mg/kg) in DMSO. 9-NP produced a significant elevation of serum aspartate aminotransferase, alanine aminotransferase, sorbitol dehydrogenase, and gamma-glutamyl transpeptidase (GGTP) levels relative to DMSO-injected rats 24 hr after injection. With the exception of GGTP, the increase in enzyme activities induced by 9-NP was significantly reduced by a 3-day pretreatment with beta-naphthoflavone (BNF; 40 mg/kg/day) in DMSO. The effect of 9-NP on GGTP levels was enhanced by BNF pretreatment.

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Male Sprague-Dawley rats were treated ip with beta-naphthoflavone (40 mg/kg/day) in corn oil or in DMSO for three days. Diphenaldehyde (90 mg/kg in DMSO) was injected ip 24 hr after pretreatment. The increase in the levels of aspartate aminotransferase, alanine aminotransferase, sorbitol dehydrogenase, gamma glutamyl transpeptidase, and lactate dehydrogenase was significantly lower in rats pretreated with BNF. This suggests that the BNF-induced P-450 isozyme systems have a protective effect against the acute hepatotoxicity of diphenaldehyde.

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Diphenaldehyde is the major product of phenanthrene ozonized on silica gel. Male Sprague-Dawley rats were treated with a single ip injection of DMSO (3.0 ml/kg) or diphenaldehyde (90 mg/kg) in DMSO. Diphenaldehyde produced significant alterations in levels of serum aspartate aminotransferase, alanine aminotransferase, sorbitol dehydrogenase, gamma-glutamyl transpeptidase, and lactate dehydrogenase relative to DMSO-injected rats 24 hr after injection. These results, as well as gross observations on necropsy, suggest that diphenaldehyde exhibits significant hepatotoxicity.

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Male Sprague-Dawley rats were treated ip with beta-naphthoflavone (BNF, 40 mg/kg/day) in dimethylsulfoxide (DMSO, 26.7 mg BNF/ml) for three days. At 24 hr after the pretreatment DMSO (3.0 ml/kg), phenanthrene (150 mg/kg), ozonized or nitrated products of phenanthrene (150 mg/kg), pyrene (150 mg/kg), or ozonized or nitrated products of pyrene (150 mg/kg) were injected ip. Phenanthrene, pyrene, and their ozonized or nitrated products were dissolved in DMSO (50 mg/ml). No increase in the level of aspartate aminotransferase (AST), alanine aminotransferase (ALT) or sorbitol dehydrogenase (SDH) was seen in the pretreated rats 48 hr after the treatment. This is in contrast to what was seen in previous work without the BNF pretreatment. BNF pretreatment induced a small but significant increase in gamma-glutamyl transpeptidase (GGTP) levels. No treatment group receiving BNF differed from another with respect to GGTP. A decrease in lactate dehydrogenase (LDH) levels was noted in the nitro-PAH treatment groups; the same phenomenon was observed earlier in rats treated with nitro-PAH without BNF treatment. These results suggest that the mixed-function oxidase systems specifically induced by BNF have a protective effect against the hepatotoxicity of the oxonized or nitrated products of phenanthrene and pyrene.

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Male Sprague-Dawley rats were treated with a single ip injection of dimethyl sulfoxide (DMSO), phenanthrene, nitrated products of phenanthrene, pyrene, or nitrated products of pyrene. Phenanthrene, pyrene and their nitrated products were dissolved in DMSO. Phenanthrene produced a significant elevation of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels relative to DMSO-injected rats 24 hr after injection. Gamma-glutamyl transpeptidase (GGTP) levels were significantly increased for groups treated with phenanthrene when compared with the DMSO group 72 hr after injection. Nitrated products of phenanthrene produced a significant elevation of serum AST, ALT, sorbitol dehydrogenase (SDH), and GGTP levels when compared with groups treated with DMSO and phenanthrene 24 hr after injection. Four of six rats in the nitrated phenanthrene treatment group died between 48 and 72 hr after the injection. Injection of pyrene caused no significant increases in serum enzyme activities. Significant changes in the serum AST, SDH and LDH levels were observed with the nitrated products of pyrene at 24 hr. Only SDH levels were significantly different when pyrene and its nitrated products were compared. No significant differences were detected at 72 hr with the nitrated products of pyrene. As supported by serum chemistry, this study suggests that the products of the reaction of NO2 with two model polynuclear aromatic hydrocarbons (PAH) are hepatotoxic. Both pyrene and phenanthrene form nitrated products that are more toxic than the parent PAH, but the nitrated products of phenanthrene appear to be more toxic than the nitration products of pyrene.

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This study was performed to investigate the possible mechanisms underlying prolongation of anesthesia times in sheep caused by the sequential administration of thiamylal and pentobarbital. Sodium thiamylal was injected as an intravenous bolus dose (13.2 mg/kg) followed in 7 min by sodium pentobarbital (14.3 mg/kg) by the same route to seven sheep. Separate studies were conducted for each of the two drugs administered separately to the same animals at the same doses. Mean anesthesia times (to the return of the palpebral reflex) were 7.89 min (thiamylal), 5.39 min (pentobarbital) and 34.1 min (the sequential combination). The kinetic parameters Vd(area), Vd(ss), t 1/2 beta, and ClB for either drug were not affected by the other when given in combination. The t 1/2 alpha was shorter, and the Vc was smaller, for pentobarbital when administered with thiamylal, while there were no changes in thiamylal disposition for the combination regimen. Computer-generated curves, associated with the two-compartment open model showing the fraction of dose in each compartment as a function of time, illustrated that pentobarbital rapidly achieved higher concentrations in the peripheral compartment after prior thiamylal administration. Protein-binding studies showed that this could not be attributed to displacement of pentobarbital from plasma albumin by thiamylal. Calculation of total and free drug concentrations at the time of awakening showed that, when the drugs were combined, the concentration of each drug was less than half of that observed at awakening when they were studied separately. It can be concluded that the prolonged sleeping times associated with the sequential combination of the two agents were not due to an alteration in kinetic parameters of either drug caused by the other, but rather to an additive effect of the subanesthetic concentrations of the two drugs when combined. The fact that sleeping times were supra-additive is attributed to a shift of awakening time from the distribution (alpha) phase, when given independently, to the elimination (beta) phase when administered in combination.

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Male Sprague-Dawley rats were treated with a single ip injection of physiological saline (3.0 ml/kg), dimethyl sulfoxide (DMSO, 3.0 ml/kg), phenanthrene (150 mg/kg), ozonized products of phenanthrene (150 mg/kg), pyrene (150 mg/kg), or ozonized products of pyrene (150 mg/kg). Phenanthrene, pyrene, and their ozonized products were dissolved in DMSO (50 mg/ml). Serum aspartate aminotransferase (AST) activity was increased significantly 24 hr after ip administration of DMSO when compared with physiological saline. Phenanthrene produced a significant elevation of serum AST and gamma-glutamyl transpeptidase (GGTP) levels related to physiological saline and DMSO-injected rats 24 hr after injection. However, GGTP levels for groups treated with DMSO or phenanthrene were not significantly increased when compared with saline groups 72 hr after injection. Ozonized products of phenanthrene produced a significant elevation of serum AST, alanine aminotransferase (ALT), GGTP, and bilirubin levels when compared with groups treated with physiological saline, DMSO, and phenanthrene 24 or 72 hr after injections. The ozonized products of phenanthrene also produced significant elevation of serum creatinine levels compared with physiological saline, DMSO, and phenanthrene groups at 24 hr after treatment and of blood urea nitrogen (BUN) levels at 24 and 72 hr. Although pyrene caused a small but significant increase in the serum AST and bilirubin levels 24 hr after treatment, no significant change in the serum AST, ALT, GGTP, BUN, and creatine levels were observed with the ozonized products of pyrene at 24 or 72 hr. This study demonstrates significant alterations in serum chemistry induced by reaction products of ozone with phenanthrene. No such effect was observed when the products of pyrene ozonation were administered. Although the ozonation products of pyrene were not toxic under the conditions of this study, phenanthrene products were more hepatotoxic than was phenanthrene itself. Nephrotoxicity was also an apparent effect of ozonized phenanthrene. Since ozone-polycyclic aromatic hydrocarbon (PAH) reactions may occur in the atmosphere, these reactions might produce compounds that are more toxic than either ozone or the PAH alone.

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A fatal case of thallium poisoning was described in a dog. Clinical signs included vomiting, gastroenteritis, and dermal lesions. Chemical analysis of urine, liver, and kidney from the dog revealed 98, 7, and 34 ppm thallium, respectively, on a wet-weight basis.

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Normal values and ranges were identified for blood lead, delta-aminolevulinic acid dehydratase, and free erythrocyte porphyrins in 104 adult female cattle in central Missouri. The blood lead mean value was 0.063 ppm with a standard deviation of 0.028. The blood delta-aminolevulinic acid dehydratase activity mean value was 45.76 U with a standard deviation of 20.57. The free erythrocyte porphyrin mean value was 21.56 micrograms coproporphyrin/100 ml erythrocytes with a standard deviation of 11.36. Analysis of variance did not reveal differences between breeds or age groups for any of the parameters. Correlation was not observed between these parameters either for the group as a whole or within breed or age groups. If lead affects delta-aminolevulinic acid dehydratase and free erythrocyte porphyrin in cattle, it is at a higher exposure level than that which existed in this sampling of adult female cattle.

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A group of 90 feeder calves was accidentally exposed to lead for approximately 30 days. The source of the intoxication was determined to be contamination of feed ingredients from a railroad car. Fourteen calves died and 8 more were clinically affected. Blood samples were obtained from 24 exposed calves (16 clinically normal and 8 intoxicated), and the samples were analyzed for lead, delta-amino levulinic acid dehydrase activity, and free erythrocyte porphyrin. Blood lead values ranged from 0.44 to 1.16 parts per million. Amino levulinic acid dehydrase activity was not affected enough to be of diagnostic value, whereas free erythrocyte porphyrin was increased dramatically and consistently in lead-exposed cattle.

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