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Biomedical subjects

K Andersson

Publications and source records attributed to K Andersson.

At least 271 records · Page 15Linked to original sources
PubMed1985

Effects of acute intermittent exposure to cigarette smoke on catecholamine levels and turnover in various types of hypothalamic DA and NA nerve terminal systems as well as on the secretion of adenohypophyseal hormones and corticosterone.

Male rats were exposed to cigarette smoke (Walton Horizontal Smoking Machine) from one to four cigarettes (Kentucky reference IR-1 type). Catecholamines in the diencephalon were measured by quantitative histofluorimetry in discrete dopamine (DA) and noradrenaline (NA) nerve terminal systems. Blood TSH, prolactin, LH, FSH, ACTH, vasopressin and corticosterone levels were determined by radioimmunoassay procedures. Exposure to unfiltered, but not to filtered (Cambridge glass fibre filters) cigarette smoke resulted in dose-dependent reductions of NA levels in the various hypothalamic NA nerve terminal systems. Evidence was obtained that exposure to unfiltered but not to filtered cigarette smoke resulted in dose-dependent increases of amine turnover (alpha MT-induced CA disappearance experiments) in the various DA and NA nerve terminal systems in the hypothalamus. The lowering of TSH, LH and prolactin secretion induced by unfiltered smoke were probably induced by nicotine and were independent of tyrosine hydroxylase inhibition. Furthermore, unfiltered cigarette smoke produced a dose-related increase in corticosterone secretion. The inhibitory effects of TSH, LH and prolactin secretion were probably in part related to the ability of unfiltered smoke via its nicotine component to activate the lateral and medial tubero-infundibular DA neurons. The increases in corticosterone secretion may at least in part be related to a smoke induced increase in the facilitatory influence of paraventricular NA nerve terminals on CRF activity.

Adrenocorticotropic Hormone↗
PubMed1985

Acute continuous exposure to cigarette smoke produces discrete changes in cholecystokinin and substance P levels in the hypothalamus and preoptic area of the male rat.

By means of a Walton Horizontal Smoking Machine, male rats were exposed to the smoke from I-4 cigarettes burned in a continuous fashion. Cholecystokinin (CCK) and substance P levels (determined by means of radio-immunoassay) were measured in discrete hypothalamic and preoptic regions. Acute continuous exposure to cigarette smoke induced increases in CCK levels in the paraventricular hypothalamic region as well as decreases in CCK levels in the median eminence. Furthermore, this treatment resulted in decreased CCK and substance P levels in the medial preoptic region. The results have been interpreted to indicate that CCK and substance P containing neuronal systems can be regulated by cholinergic nicotine-like receptors.

Animals↗
PubMed1985

Mecamylamine pretreatment counteracts cigarette smoke induced changes in hypothalamic catecholamine neuron systems and in anterior pituitary function.

We have studied the effects of acute, intermittent exposure to tobacco smoke on discrete hypothalamic CA nerve terminal networks and on neuroendocrine function by means of quantitative histofluorimetrical determinations of catecholamine (CA) fluorescence in sections of rat brain and by radioimmunoassay procedures for hormones. Acute intermittent exposure to cigarette smoke induced a lowering of NA levels and increased NA turnover in discrete hypothalamic nerve terminal regions. This exposure also induced increases in DA turnover in the median eminence. The cigarette smoke lowered TSH, prolactin, LH and FSH serum levels, but induced an increase in serum corticosterone concentrations. To determine if the above mentioned changes in neuroendocrine function were nicotine mediated, a cholinergic nicotine-like blocking agent, mecamylamine, was administered prior to exposure to cigarette smoke. Pretreatment with mecamylamine (1.0 mg kg-1) counteracted the cigarette smoke induced changes in CA levels and turnover in all hypothalamic CA nerve terminal regions as well as the changes in serum levels of the pituitary hormones and corticosterone. It is suggested that acute intermittent exposure to cigarette smoke, via its nicotine component, lowers TSH, prolactin, LH and FSH secretion at least in part through activation of the tubero-infundibular DA neurons. Furthermore, the nicotine component of the cigarette smoke is suggested to induce the increase in corticosterone serum levels via increasing NA turnover in the paraventricular hypothalamic nucleus.

Animals↗
PubMed1985

Cholecystokinin neuron systems and their interactions with the presynaptic features of the dopamine neuron systems. A morphometric and neurochemical analysis involving studies on the action of cholecystokinin-8 and cholecystokinin-58.

A unique role for CCK-58 compared to that for CCK-8 has been demonstrated in the modulation of central catecholaminergic mechanisms and neuroendocrine functions. It is of paramount importance to localize CCK-58 immunoreactivity within the brain in order to establish if separate CCK-58- and CCK-8-immunoreactive neuron systems exist. The two most significant actions of CCK-58 are a marked lowering of TSH secretion and a selective increase of DA turnover in DA-CCK co-existing synapses in the nucleus accumbens and tuberculum olfactorium.

Animals↗
PubMed1985

Cancer mortality of cadmium workers.

Several epidemiological studies of workers exposed to cadmium indicate an increased risk of lung and prostatic cancer. The increase is statistically significant in some of the studies but the SMR is greater than 100 in almost all. A cohort study of the mortality among 522 Swedish workers exposed to cadmium for at least one year in a nickel-cadmium battery plant support the earlier findings. The SMR for lung and prostatic cancer increased with increasing dose and latency but did not obtain statistical significance. A combination of all the available data from the most recent follow up of causes of death among cadmium workers in six different cohorts shows 28 cases of prostatic cancer (SMR = 162) and 195 cases of lung cancer (SMR = 121). This new analysis suggests that long term, high level exposure to cadmium is associated with an increased risk of cancer. The role of concomitant exposure to nickel needs further study.

Cadmium↗
PubMed1985

The effects of acute and chronic treatment with triiodothyronine and thyroxine on the hypothalamic and telencephalic catecholamine nerve terminal systems of the hypophysectomized male rat. Chronic treatment modulates catecholamine utilization in discrete catecholamine nerve terminal systems.

Using catecholamine (CA) fluorescence histochemistry in combination with quantitative microfluorimetry, it has been shown that chronic treatment with triiodothyronine (T3) and thyroxine (T4; 2 X 10 and 2 X 36 micrograms/kg i.p., respectively, twice daily for 10 days), but not acute treatment (1 and 3.6 mg/kg i.p., respectively, 2 h before killing), increases CA utilization in the medial and lateral palisade zones of the median eminence and reduces noradrenaline (NA) utilization in the parvocellular part and magnocellular part of the paraventricular hypothalamic nucleus of the hypophysectomized male rat. Following chronic T4 treatment it could also be shown that the CA levels in the medial and lateral palisade zones of the median eminence were increased, while the NA levels were reduced in the parvocellular part of the paraventricular hypothalamic nucleus. Chronic T3 treatment induced similar changes - increased CA levels in the medial palisade zone and reduced NA levels in the magnocellular part of the paraventricular hypothalamic nucleus. Within the telencephalon, chronic but not acute treatment with T3 or T4 selectively increased dopamine (DA) utilization within the diffuse type of DA nerve terminal systems of the nucleus accumbens. This action of chronic treatment of T3 or T4 was highly selective and no changes in DA levels could be demonstrated in any DA nerve terminals analyzed in the nucleus caudatus putamen; nucleus accumbens and tuberculum olfactorium. In all the experiments the TSH levels remained undetectable and the low basal serum prolactin levels were not modulated in any experimental group in spite of the treatment with a tyrosine hydroxylase inhibitor in the CA utilization experiments. Following 2-3 weeks after hypophysectomy, serum T3 and T4 were decreased by 30-50%. In the acute experiments with T3 or T4, serum T3 levels and T3 as well as T4 levels were markedly elevated after the respective treatments. In the chronic experiments, the T4 treatment resulted in significant increases in the serum levels of both T3 and T4. The present results indicate that discrete DA and NA nerve terminal systems within the median eminence (DA), nucleus accumbens (DA) and paraventricular hypothalamic nucleus (NA) can slowly respond to chronic treatment with T3 or T4. This effect is the result of a direct action of the thyroid hormones on the brain since TSH is absent in the hypophysectomized rat.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

Effects of chronic exposure to cigarette smoke on amine levels and turnover in various hypothalamic catecholamine nerve terminal systems and on the secretion of pituitary hormones in the male rat.

Male rats were exposed to the smoke from 2 cigarettes every morning for a total-period of 9 days. The next day they were decapitated immediately after the exposure to the smoke from 4 cigarettes (Kentucky reference IR-1 type) burned at 30-min intervals. Control animals were exposed to air alone or to nicotine-free cigarette smoke (Cambridge glass fibre filters). In contrast to chronic exposure to filtered smoke, exposure to unfiltered smoke resulted in a 10% increase in catecholamine (CA) levels (quantitative histofluorimetry) within the lateral palisade zone, the posterior periventricular hypothalamic nucleus and within the dorsomedial hypothalamic nucleus. There was also an increase in amine turnover (tyrosine hydroxylase inhibition by alpha-methyl-dl-p-tyrosine methylester; alpha MT) in the dopamine (DA) systems of the medial and lateral palisade zones and in the periventricular noradrenaline (NA) hypothalamic systems. Chronic exposure to unfiltered cigarette smoke resulted in reductions of prolactin, LH and FSH levels (radioimmunoassay). Following alpha MT treatment chronic exposure to unfiltered cigarette smoke still led to reduced prolactin serum levels. In addition an increased vasopressin serum concentration was found. The effects of chronic exposure to cigarette smoke on neuroendocrine function and on hypothalamic CA systems are suggested to be mediated via nicotine. Combined with the results from a previous study the present results indicate that tolerance does not develop with regard to the inhibitory effects of exposure to cigarette smoke on prolactin, LH and FSH secretions. The same is true for the stimulatory effects on the tubero-infundibular DA neurons and the periventricular NA systems. But chronic exposure to cigarette smoke seemed to induce tolerance with regard to its stimulatory effects on subependymal, dorsomedial and paraventricular hypothalamic NA systems and on corticosterone release.

Adrenocorticotropic Hormone↗
PubMed1984

Luteinizing hormone-releasing hormone increases dopamine turnover in the lateral palisade zone of the median eminence and reduces noradrenaline turnover in the nuc. preopticus medialis of the hypophysectomized male rat.

By means of catecholamine fluorescence histochemistry in combination with quantitative microfluorimetry the effects of luteinizing hormone-releasing hormone (LH-RH) has been studied on the amine levels and turnover in discrete catecholamine (CA) nerve terminal populations in the hypothalamus of the hypophysectomized male rat. LH-RH highly selectively increases dopamine (DA) turnover in the lateral palisade zone of the median eminence and highly selectively reduces noradrenaline turnover in the nucleus preopticus medialis without influencing amine levels in these CA nerve terminal systems. It is suggested that the ultrashort feed-back action of LH-RH involves increased release of DA in the lateral palisade zone leading to activation of the DA receptor inhibiting LH-RH release as well as a reduced noradrenaline release in the nucleus preopticus medialis leading to a reduced excitatory influence on the LH-RH neurons at the soma-dendritic level.

Animals↗
PubMed1984

Isopycnic centrifugation of rat-liver microsomes in isoosmotic gradients of Percoll and release of microsomal material by low concentrations of sodium deoxycholate.

Rat-liver microsomes were subjected to isopycnic centrifugation under isoosmotic conditions in gradients of Percoll containing 0%, 0.05%, 0.1% and 0.2% sodium deoxycholate, respectively. The buoyant density of the microsomes was in the range 1.043 to 1.046 g/ml, independent of the detergent concentration. Absorbance measurements and polyacrylamide gel electrophoresis revealed that the detergent causes an increase in the release of material from the microsomes. Electron microscopy studies showed that membrane disassembly was avoided if the microsomes were isolated at concentrations below 0.1% sodium deoxycholate.

Animals↗
PubMed1984

Central catecholamine neurons and exposure to dichloromethane. Selective changes in amine levels and turnover in tel- and diencephalic DA and NA nerve terminal systems and in the secretion of anterior pituitary hormones in the male rat.

Subacute exposure of male rats to various concentrations (70-1000 ppm) of dichloromethane (DCM) produces a selective reduction of dopamine (DA) levels without a change of DA turnover in certain types of forebrain DA nerve terminal systems. In the low concentration (70 ppm) a selective reduction of DA turnover was observed in the medial palisade zone (MPZ) of the median eminence. This chlorinated organic solvent also produced a discrete dose-dependent increase of noradrenaline (NA) turnover within the anterior periventricular hypothalamic area and with the highest concentration an increase of NA turnover in the anteromedial frontal cortex. DCM reduced NA levels dose-dependently in the posterior periventricular hypothalamic area and also reduced NA levels in the dorsomedial hypothalamic nucleus (1000 ppm). Following tyrosine hydroxylase inhibition DCM produced an inversely dose-related increase of serum LH levels and at the highest concentration an increase of ACTH secretion was observed. It is suggested that DCM can produce discrete changes in amine storage and turnover in catecholamine (CA) nerve terminal systems of the tel- and diencephalon, some of which may contribute to the DCM induced disturbances of the secretion of anterior pituitary hormones but actions on other transmitter-identified neurons involved in neuroendocrine regulation must also be considered.

Animals↗
PubMed1984

Packing of a specific gene into higher order structures following repression of RNA synthesis.

Transcription of the Balbiani ring (BR) genes of the dipteran Chironomus tentans was inhibited by teh nucleoside analogue DRB (5,6-dichloro-1-beta-D-ribofuranosyl benzimidazole). The BR genes were emptied of RNA polymerases and the subsequent packing of the genes was monitored by transmission electron microscopy. The thin chromatin axis of the transcriptionally active genes condensed into a thick (20-25 nm) chromatin fiber, which was recorded as a linear structure, an open loop or a supercoiled loop. The compacted genes were finally packed into dense clumps of chromatin. It was proposed that upon repression of RNA synthesis the BR gene template attains the following consecutive stages with increasing compaction: transcription loop----linear thick fiber----open thick fiber loop----supercoiled thick fiber loop----dense chromatin. Within the chromatin blocks structures that resembled the supercoiled loops were discerned, suggesting that the final packing of the template might be accomplished by a close alignment of supercoiled loops.

Animals↗
PubMed1984

A new method for the analysis of tetramethyllead in blood.

In this paper a method for the determination of alkyllead compounds in blood is described. The method is based on extraction of the aklyllead compounds into an organic solvent, followed by separation by high-resolution gas chromatography. A graphite-furnace atomic absorption spectrophotometer is used as the detector. A detection limit of 0.01 micrograms/ml for tetramethyllead was obtained in blood samples. The method was used for the investigation of occupational exposure to tetramethyllead in gasoline. Blood samples from tank cleaners and gasoline pump servicemen showed detectable amounts of tetramethyllead. The reference group did not show any detectable levels of tetramethyllead.

Chromatography, Gas↗
PubMed1983

Evidence for the existence of a dopamine receptor of the D-1 type in the rat median eminence.

By means of receptor autoradiography using the dopamine (DA) receptor radioligands [3H]cis(z)-flupenthixol ([3H]FLU), [3H]spiperone, [3H]N-propyl-norapomorphine and amino-6,7-dihydroxy-1,2,3,4-tetrahydronaphtalene-2-(5,8[3H]) in combination with a microdensitometrical analysis indications have been obtained for the existence of a DA receptor of the D-1 type in the median eminence of the male rat. Thus, only [3H]FLU (10-20 nM) strongly labeled both the nuc. caudatus putamen and the median eminence and the labeling was markedly prevented by (+)-butaclamol in both regions. Furthermore, a DA receptor agonist of the D-1 type preferentially displaced [3H]FLU from the median eminence. Thus, a DA receptor of the low affinity type may regulate the secretion of hypothalamic hormones from the median eminence.

Animals↗
PubMed1983

Rat growth hormone and hypothalamic catecholamine nerve terminal systems. Evidence for rapid and discrete reductions in dopamine and noradrenaline levels and turnover in the median eminence of the hypophysectomized male rat.

Rat growth hormone (rGH) (100 micrograms/kg) produced 2-4 h after its i.v. injection a rapid reduction of catecholamine stores and turnover in the subependymal layer and in the medial and lateral palisade zone of the median eminence. It is suggested that rGH may inhibit its own secretion partly via reduction of DA synthesis and release in the median eminence leading to increased somatostatin release and partly via reduced noradrenaline synthesis and turnover in the median eminence leading to reduced secretion of a growth hormone releasing factor.

Animals↗
PubMed1983

Rapid and discrete changes in hypothalamic catecholamine nerve terminal systems induced by audiogenic stress, and their modulation by nicotine-relationship to neuroendocrine function.

The effects of acute audiogenic stress, with or without simultaneous nicotine treatment (0.3 mg/kg i.v.), on catecholamine levels in discrete dopamine and noradrenaline nerve terminal systems of the hypothalamus, and on the secretion of adenohypophyseal hormones and of corticosterone, were studied using quantitative microfluorometric evaluations of catecholamine stores and radioimmunoassays for the determination of serum hormone levels. Audiogenic stress and nicotine induced very rapid and discrete decreases in noradrenaline levels in the subependymal layer (SEL), in the parvocellular part of nuc. paraventricularis hypothalamic (PA FP) and in the posterior periventricular hypothalamic systems, (PV II); the decreases were apparent 2 min following the onset of treatment. Increases of arterial blood pressure were observed after nicotine treatment but could not have been a major factor in producing the changes in catecholamine levels. These changes in NA levels may be related to the nicotine- and stress-induced increases of ACTH (SEL and PA FP) and prolactin secretion (PV II) found in the present experiments. Stress enhanced the rapid but variable increase in vasopressin secretion induced by nicotine, suggesting one possible mechanism by which stress combined with smoking can contribute to the development of increased arterial blood pressure and finally to sustained hypertension.

Animals↗