Müller cell involvement in methanol-induced retinal toxicity.

Methanol is an ocular toxicant which causes visual dysfunction often leading to blindness after acute exposure. The physiological and biochemical changes responsible for this toxicity are poorly understood. Previously, we reported that the folate-reduced (FR) rat is an animal model which mimics the characteristic human methanol toxicities.

Role of retinal metabolism in methanol-induced retinal toxicity.

Methanol is a toxicant that causes systemic and ocular toxicity after acute exposure. The folate-reduced (FR) rat is an excellent animal model that mimics characteristic human methanol toxic responses. The present study examines the role of the methanol metabolites formaldehyde and formate in the initiation of methanol-induced retinal toxicity.

Myelotoxic, neurotoxic and reproductive adverse effects of nitrous oxide.

N2O is a relatively safe general anaesthetic under normal medical and dental anaesthetic use. It is more likely to produce megaloblastosis or neuropathy when used repetitively or for periods longer than 3 hours or in individuals with vitamin B12 deficiencies. The mechanism responsible for its myelotoxicity, neurotoxicity and most likely its reproductive toxicity, involves its inhibition of MetSyn and the resulting reduction in SAM and THF levels.

Diminished mephobarbital anticonvulsant action following diphenhydramine pretreatment.

Diphenhydramine and other antihistamines produce biphasic effects on drug disposition and lower seizure threshold, thereby potentially diminishing the efficacy of anticonvulsants such as mephobarbital. Accordingly, the influence of diphenhydramine (50 mg/kg, IP) pretreatment on the anticonvulsant activity of mephobarbital (50 mg/kg, IP) was determined in adult female Swiss-Webster mice given pentylenetetrazol (SC). Diphenhydramine lowered the pentylenetetrazol convulsive dose (CD50) by 60%.

Erythrocyte pyrimidine 5'-nucleotidase inhibition by acute lead exposure in neonatal rats.

Inhibition by lead of erythrocyte pyrimidine 5'-nucleotidase (P5N) is thought to contribute to morphological abnormalities observed in red blood cells (RBC) of lead-exposed subjects. However, neither the mechanism of lead inhibition of P5N nor the relationship of this inhibition to blood lead levels attained in exposed subjects is known. In the present investigation, acute in vivo and in vitro lead acetate effects on erythrocyte P5N from 21-day-old rat pups were determined and were related to blood lead concentrations ascertained by atomic absorption spectrophotometry.

Discriminative stimulus properties of amphetamine and other stimulants in lead-exposed and normal rats.

The present study examined the discriminative stimulus properties of amphetamine (AMP) at progressively lower doses in lead-exposed and normal rats. In addition, generalization gradients of AMP, apomorphine, methylphenidate, and caffeine to both high and low training doses of AMP were determined in these rats. Under the high AMP training dose condition (1.

Age of testing as a factor in the behavioral effects of early lead exposure in rats.

The behavioral effects of postnatal administration of lead during weaning were tested in young and adult rats. Rats received either 10 mg/kg IP lead acetate or equimolar sodium acetate daily for the first twenty days of life. Tests of performance on an 8-arm radial maze and a passive avoidance task were begun at 25 days after birth or 90 days after birth.

Differential effects of folic acid on water content, protein and microsomal 5'-phosphodiesterase activity of the rat kidney.

The effects of folic acid administration on the weight, protein, water content and microsomal 5'-phosphodiesterase of the rat kidney were determined, to elucidate the mechanisms contributing to the renal enlargement produced by this agent. Folic acid administered ip in single doses of 100-250 mg/kg caused dose-related increases in kidney weight, water and protein content within 24 hr. Time-course studies indicated that 250 mg folic acid/kg given ip produced a progressive elevation in renal water content from 2 to 72 hr.

Effect of lead acetate on the kinetics of gamma-glutamyl transpeptidase activity from neonatal rat pup brain.

The objective of the present investigation was to determine the influence of lead acetate on kinetic parameters of gamma-Glutamyl Transpeptidase (GGT) in brain homogenates from 15 and 30 day old rat pups. Determinations of maximal velocity (Vmax) indicated that the Vmax of GGT from 15 day old pups was 58% of that from 30 day old animals while negligible differences in apparent Km were observed between either group. Addition of lead acetate to GGT preparations from 15 day old pups produced no significant changes in apparent Km for gamma-Glutamyl-p-Nitroanilide (GPNA).

P-Chloro-N-methylaniline demethylation by rat kidney subcellular fractions.

Subcellular fractions prepared from kidney homogenates catalyzed the demethylation of p-chloro-N-methylaniline (PCMA). The activity of the renal preparations were forty-one percent of the liver 9,000 xg supernatant fraction activity. A differential susceptibility to the addition of carbon monoxide, p-chloromercuribenzoate or the omission of NADPH and magnesium characterized the two preparations.