[The incisor of the rat--not only an indicator for disorders of homeostasis]. / Der Schneidezahn der Ratte--nicht allein ein Indikator für Störungen der Homöostase.

In experimental endocrinology and for studies of disturbed homeostasis caused by alterations of mineral metabolism rat incisors are known test model. Recently they will be relevant to interpret effects of xenobiotics. In our experiments we found remarkable correlations between specific organ toxicity (affinity) and histotropic effects in the incisors (enamel or dentine), further variations of the reaction in relation to the time of application.

[Effect of metabolic changes in the liver on the cytotoxic activity of cyclophosphamide in the incisor of rats]. / Wirkung metabolischer Zustandsänderungen der Leber auf die zytotoxische Aktivität von Zyklophosphamid am Schneidezahn der Ratte.

The incisor of the rat is a sensitive biological indicator which records nutritive and hormonal disorders as well as toxic influences. The present investigation was aimed to provide information whether or not the manifestation of cyclophosphamide-caused hypoplasias could be altered by an induction (phenobarbital) or inhibition (carbon tetrachloride) of the liver biotransformation capacity. Cyclophosphamide (15 or 30 mg/kg) was injected intraperitoneally. Pretreatment of the rat with phenobarbital produced an increase (35%) of the malformation, whereas carbon tetrachloride led to a dose dependent decrease (30 or 50%). Our investigations suggest that the cyclophosphamide induced defect of the incisor is due to an alteration of the metabolic liver function.

Effect of carbon monoxide exposure on heart cytochrome c oxidase activity of rats.

The activity of cytochrome c oxidase in heart muscle of rats was within the control range 1 and 24 h after commencement of CO exposure (56% COHb) and was significantly decreased 3 h thereafter. A decrease of the enzyme activity was also detectable 3 h following repeated CO exposure demonstrating that cytochrome c oxidase does not seem to play a role in the adaptive response of organism to chronic CO exposure.

[Stressor effect of toxins]. / Zur stressorischen Wirkung von Schadstoffen.

The organism reacts in a different way to contamination by damaging agents. Chemical stressors enforce the organism to develop adaptive reactions. In the field of industrial medicine the objectivation of premorbid phases is of particular importance.

Seasonal variations of carbon monoxide-induced polycythemia in rats.

Fluctuations of the extent of polycythemia in rats due to repeated exposure to carbon monoxide prompted us to study whether the differences were caused by seasonal variations. Data from 18 independent experiments involving the hemoglobin values of 206 CO-exposed and 208 control rats over a period of nearly 3 years were available. Because the experiments were not designed for chronobiological studies, several methods of quasilinear and nonlinear regression analysis were applied to fit periodic models to the data. The best fit was obtained by a single cosine function with a period of nearly 12 months and with maximum values in winter and minimum values in summer. Experiments to elucidate mechanism(s) of seasonal variations showed that following a single CO exposure to the nocturnally active rodents, the rate of CO release from the body was higher in the dark span, that reduced food supply produced a potentiation of the CO-induced hemoglobin increase, and that the adaptive CO response was not affected by testosterone or thyroidectomy, but inhibited by L-thyroxine. Thus it seems that influences of light, CO elimination rate, food intake, metabolic rate and related hormones play a role for seasonal variations.

[Neuropathies following carbon monoxide poisoning]. / Neuropathien nach Kohlenmonoxidvergiftungen.

According to the experiments carried out in animals, impairments of the peripheral nerves can, with a certain regularity, also be expected in patients in the presence of the respective high degree of carbon monoxide intoxications without clinical paralytic symptoms being detectable in every case. The changes in the motor nerve conduction velocity in our patients and in animal experiments are still found over a prolonged period of time after the acute intoxication.

[Animal experiments and clinical observations on poisoning with metallic mercury]. / Tierexperimentelle und klinische Beobachtungen zur Intoxikation durch metallisches Quecksilber.

Albino rats of an own culture strain exposed to mercury were investigated electroneurographically. A disturbance of the motor nerve conduction of the ischiadic and the tibial nerve could not be established after one year. Workers exposed to mercury of two chemical plants of the district of Halle were examined neurologically and electrophysiologically. The motor nerve conduction was measured on eight peripheral nerves. The measuring values above all deviate from the normal value up to 10% more infrequently up to 20% or more.

[Hg concentrations in blood and organs of the rat following Hg contamination of the skin]. / Hg-Konzentrationen in Blut und Organen von Ratten nach langfristiger Hg-Kontamination der Haut.

Metallic mercury was applied as ointment to the skin of rats. The mercury concentrations recorded from blood, kidneys, and urine suggested that metallic mercury was properly absorbed through the skin.

Effect of dichloromethane on the sciatic motor conduction velocity of rats.

There is a correlation between dichloromethane dosis (X) of 1--6 mmole/kg administered i.p. to rats and the sciatic motor conduction velocity (Y): Y = 57.1--1.091 X. The correlation coefficient 'r' is 0.437 (p less than 0.01). Presumably, the decrease of nerve conduction velocity is caused by the endogenous carbon monoxide production due to dichloromethane biotransformation.

Effect of repeated carbon monoxide intoxications on the myoglobin concentration in heart and skeletal muscle of rats.

A study was made to determine whether or not myoglobin plays a role in the adaptation response of an organism to chronic carbon monoxide exposure. Rats were injected subcutaneously with carbon monoxide (2.4 and 7.2 mmol CO/kg body weight, once daily on 5 days a week) 30times, 60times, or 107times. These exposure conditions resulted in carboxyhemoglobin concentrations of about 45 and 60%, respectively, as well as in an increase in both the hemoglobin concentration and the hematocrit. In skeletal muscle the myoglobin concentrations were not changed significantly, whereas the heart muscle showed an increase mean myoglobin concentration after the prolonged CO hypoxia (7.2 mmol CO/kg, 107times) by 54%.

Urinary catecholamine excretion and blood sugar response during acute poisonings with dinitrobenzenes.

Rats were injected intraperitoneally with 0.015 mmol of p-dinitrobenzene/kg, 0.15 mmol of m-dinitrobenzene/kg and 0.45 mmol of o-dinitrobenzene/kg body wt. The dinitrobenzenes induced methaemoglobin concentrations of 86%, 60% and 49%, respectively, as well as increases of urinary catecholamine excretion and blood sugar concentration. Due to hyperglycaemia the glycolysis may be stimulated as mechanism for energy production in methaemoglobin-induced oxygen deficiency and as mechanism for reduction of methaemoglobin, that means as responses favouring survival after poisoning.