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Biomedical subjects

A Schaffer

Publications and source records attributed to A Schaffer.

14 recordsLinked to original sources
PubMed1996

Effects of exposure to lead on selected biochemical and haematological variables.

Blood and urine samples were taken from 34 persons occupationally exposed to lead and from 56 non-exposed control persons and blood lead and haemoglobin concentrations, red blood cell count, erythrocyte glutathione peroxidase (GSH-peroxidase) and acetylcholinesterase (AChE), and urinary delta-aminolevulinic acid were determined. Blood lead concentrations of the lead-exposed subjects were within the range of generally accepted as safe for occupationally-exposed adults in many countries (i.e. below 50 micrograms Pb/dl blood). Yet, significant dose-dependent elevations were found in erythrocyte GSH-peroxidase and urinary delta-aminolevulinic acid. The urinary delta-aminolevulinic acid concentration of lead-exposed smokers was significantly elevated over that of lead-exposed non-smokers. Smoking did not effect the urinary delta-aminolevulinic acid concentration of control persons. In addition, a statistically significantly lower red blood cell count was observed in the lead-exposed group. Our results indicate that the above described safety standard for blood lead concentrations in occupationally exposed adults, although generally accepted, needs revision.

Acetylcholinesterase↗
PubMed1995

UV irradiation and heat shock mediate JNK activation via alternate pathways.

To elucidate cellular pathways involved in Jun-NH2-terminal kinase (JNK) activation by different forms of stress, we have compared the effects of UV irradiation, heat shock, and H2O2. Using mouse fibroblast cells (3T3-4A) we show that while H2O2 is ineffective, UV and heat shock (HS) are potent inducers of JNK. The cellular pathways that mediate JNK activation after HS or UV exposure are distinctly different as can be concluded from the following observations: (i) H2O2 is a potent inhibitor of HS-induced but not of UV-induced JNK activation; (ii) Triton X-100-treated cells abolish the ability of UV, but not HS, to activate JNK; (iii) the free radical scavenger N-acetylcysteine inhibits UV- but not HS-mediated JNK activation; (iv) N-acetylcysteine inhibition is blocked by H2O2 in a dose-dependent manner; (v) a Cockayne syndrome-derived cell line exhibits JNK activation upon UV exposure, but not upon HS treatment. The significance of Jun phosphorylation by JNK after treatment with UV, HS, or H2O2 was evaluated by measuring Jun phosphorylation in vivo and also its binding activity in gel shifts. HS and UV, which are potent inducers of JNK, increased the level of c-Jun phosphorylation when this was measured by [32P]orthophosphate labeling of 3T3-4A cultures. H2O2 had no such effect. Although H2O2 failed to activate JNK in vitro and to phosphorylate c-Jun in vivo, all three forms of stress were found to be potent inducers of binding to the AP1 target sequence. Overall, our data indicate that both membrane-associated components and oxidative damage are involved in JNK activation by UV irradiation, whereas HS-mediated JNK activation, which appears to be mitochondrial-related, utilizes cellular sensors.

3T3 Cells↗
PubMed1995

Visual evoked potentials N75 and P100 latencies correlate with urinary delta-aminolevulinic acid, suggesting gamma-aminobutyric acid involvement in their generation.

Pattern reversal visual evoked potentials were recorded from 31 subjects who were occupationally exposed to lead and 54 non-exposed controls. No significant effects of lead were observed in the general subject population. However, when only non-smokers (17 lead-exposed and 27 controls) were evaluated, significant effects were found. The P100, but not the N75, latency was significantly prolonged in the lead-exposed group, and this correlated with both blood lead level and age. Nevertheless, both the N75 and P100 latencies correlated with the concentration of delta-aminolevulinic acid (delta-ALA) in urine and age. This, at least in part, could be due to elevated delta-ALA levels competing at gamma-aminobutyric acid (GABA) receptor neurons. This is consistent with the fact that GABA receptor neurons are involved along the entire length of the visual pathway. The results indicate that lead affects neural function even at permitted levels of exposure, and that this level should be reduced.

Aminolevulinic Acid↗
PubMed1995

The effect of lead exposure on target detection and memory scanning differs.

Visual event-related potentials were measured in lead-exposed and control subjects, while they were performing a target detection as well as a memory scanning task. Blood lead and urinary delta-aminolevulinic acid (delta-ALA) were determined in samples taken on the same day. Lead exposure did not affect the memory scanning P300 latency, but it did delay the target detection P300 latency in a dose-dependent fashion. The P300 amplitude of lead-exposed subjects was significantly reduced for both tasks, but not in a dose-dependent fashion. The target detection, but not the memory scanning, P300 latency correlated with urinary delta-ALA. No correlation of P300 with age was found, even though the subjects ranged from 20 to 60 years of age. The difference in the effect of lead exposure on the target detection and memory scanning P300 adds to the evidence that the P300 for the two tasks arises from different generators. The absence of a correlation of the measured P300 latency for each task with age in the present study raises the possibility that this extensively reported observation might, in part, be due to inappropriately matched younger and older subjects. This study indicates that evaluation of subjects exposed to toxic substances can increase our basic understanding of evoked potentials, as well as providing evidence of their toxic manifestations.

Analysis of Variance↗
PubMed1994

A multidisciplinary study of lead-exposed subjects. I. Delayed target detection P-300 latency, an electrophysiological parameter, correlates with urinary delta-ALA.

Visual event-related potentials, generated while performing a target detection (oddball) task, were successfully evaluated in 21 out of 34 individuals occupationally exposed to lead and 40 out of 56 nonexposed controls who were examined. The blood lead level of the lead-exposed subjects ranged from a mean of 29 to 53 micrograms Pb/dl blood in three exposed subgroups, while that of the control group was 7.7 micrograms Pb/dl blood. The latencies of the N2 and P300 components of the visual event-related potential were significantly longer in the lead-exposed subjects. Both the N2 and P300 latencies significantly correlated with the blood lead levels of the subjects. In addition, the P300 latency correlated with the concentration of delta-aminolevulinic acid (delta-ALA) in urine. This in part could be due to elevated delta-ALA levels interacting with gamma-aminobutyric acid (GABA) receptor neurons. The results indicate that lead affects mental function even at permitted levels of exposure. They strengthen the conclusion, based on biochemical and hematological assays, that the maximum permitted blood lead level of 50 micrograms Pb/dl blood is not safe and should be reduced.

Adult↗
PubMed1988

A simplified low iodine diet in I-131 scanning and therapy of thyroid cancer.

A simplified, low iodine diet was developed for outpatient use prior to I-131 scanning and therapy in thyroid cancer. Iodine intake of five subjects on the diet was approximately 50 micrograms a day and this level was maintained for four weeks. The diet required only minimal instruction to be followed reliably. This level of iodine intake may increase radioiodine uptake in thyroid carcinomas.

Adult↗
PubMed1983

[A case of carbon tetrachloride poisoning].

The authors present a case of severe poisoning as a result of ingestion of a considerable amount of Carbon Tetrachloride, where toxic hepatitis and hepato-nephritis, neurological occurrences and sexual disturbances appeared. There was a considerable decline of the libido, complete impotence during several months. The accident occurred owing the ignorance of the instructions, unlabelled toxic material as such and not keeping it in a safe place. The Hamsin - a hot and dry wind - played an important part in the quick and severe appearance of the poisoning. The sexual disturbances which did not exist before the poisoning, appeared immediately after the intoxication. They were apparently connected with the injury of the liver cells; they are similar to those induced under the influence of other toxic materials. The general condition, including the sexual disturbances improved, and patient returned to his normal working condition after a period of nine months.

Adult↗