Acute noise stress, ACTH administration, and blood pressure alteration

Gamallo, A.; Alario, P.; Gonzalez-Abad, M.J.; Villanúa, María Ángeles

doi:10.1016/0031-9384(92)90309-p

Cited by 16 publications

(11 citation statements)

References 42 publications

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“…Doses of ACTH known to provoke corticosterone secretion in the rat are at least 15 IU kg −1 (e.g. Gamallo et al, 1992) or 50-500 µg kg −1 (e.g. Turner et al, 1998) administered subcutaneously.…”

Section: Establishing Adrenal Competence: a Proposed In Vivo Study Dementioning

confidence: 99%

Adrenal toxicology: a strategy for assessment of functional toxicity to the adrenal cortex and steroidogenesis

Harvey

Everett

Springall

2007

J of Applied Toxicology

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The adrenal is the most common toxicological target organ in the endocrine system in vivo and yet it is neglected in regulatory endocrine disruption screening and testing. There has been a recent marked increase in interest in adrenal toxicity, but there are no standardised approaches for assessment. Consequently, a strategy is proposed to evaluate adrenocortical toxicity. Human adrenal conditions are reviewed and adrenocortical suppression, known to have been iatrogenically induced leading to Addisonian crisis and death, is identified as the toxicological hazard of most concern. The consequences of inhibition of key steroidogenic enzymes and the possible toxicological modulation of other adrenal conditions are also highlighted. The proposed strategy involves an in vivo rodent adrenal competency test based on ACTH challenge to specifically examine adrenocortical suppression. The H295R human adrenocortical carcinoma cell line is also proposed to identify molecular targets, and is useful for measuring steroids, enzymes or gene expression. Hypothalamo-pituitary-adrenal endocrinology relevant to rodent and human toxicology is reviewed (with an emphasis on multi-endocrine axis effects on the adrenal and also how the adrenal affects a variety of other hormones) and the endocrinology of the H295R cell line is also described. Chemicals known to induce adrenocortical toxicity are reviewed and over 60 examples of compounds and their confirmed steroidogenic targets are presented, with much of this work published very recently using H295R cell systems. In proposing a strategy for adrenocortical toxicity assessment, the outlined techniques will provide hazard assessment data but it will be regulatory agencies that must consider the significance of such data in risk extrapolation models. The cases of etomindate and aminoglutethimide induced adrenal suppression are clearly documented examples of iatrogenic adrenal toxicity in humans. Environmentally, sentinel species, such as fish, have also shown evidence of adrenal endocrine disruption attributed to exposure to chemicals. The extent of human sub-clinical adrenal effects from environmental chemical exposures is unknown, and the extent to which environmental chemicals may act as a contributory factor to human adrenal conditions following chronic low-level exposures will remain unknown unless purposefully studied.

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Section: Establishing Adrenal Competence: a Proposed In Vivo Study Dementioning

confidence: 99%

Adrenal toxicology: a strategy for assessment of functional toxicity to the adrenal cortex and steroidogenesis

Harvey

Everett

Springall

2007

J of Applied Toxicology

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“…Corticosterone levels were kindly measured by Dr. M.A. Villanfla, using a specific radioimmunoassay technique, with hydroxyapatite as a new method of separating the free and bound phases, as previously described (Villanfla and Gamallo 1985;Gamallo et al 1992). …”

Section: Animals Female Virgin Rats Of the Wistar Strain (> 8 Weeks mentioning

confidence: 99%

Sex-dimorphic psychomotor activation after perinatal exposure to (−)-Δ9-tetrahydrocannabinol. An ontogenic study in wistar rats

1994

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The ontogeny and the adult expression of motor behaviors were studied in male and female rats born from mothers exposed to delta 9-tetrahydrocannabinol (THC, 5 mg/kg) during gestation and lactation. Perinatal exposure to THC increased both rearing and locomotor activities in males and females at immature preweanling ages (P-15 and P-20). These effects disappeared after ceasing THC exposure (postweaning ages), but they were observed again in adult (P-70) females. The effects appeared as persistently high motor activity in familiar environments, disappearing the characteristic habituation profile in locomotor and exploratory behaviors. In novel environment condition tests, adult (P-70) THC-exposed females, but not males, exhibited lower locomotor activity in the socio-sexual approach test, and an increase in the emergence latency in the dark-light emergence test. Additionally, animals of both sexes exposed to THC showed a increase in the time spent grooming measured in novelty conditions. These findings suggest that perinatal exposure to THC affects both the development and the adult expression of motor behaviors and it resulted in a sex-dimorphic psychomotor activation very similar to that observed after perinatal exposure to other drugs of abuse. A possible role of THC-induced pituitary-adrenal (PA) axis activation was also evaluated by measuring plasma corticosterone levels in adult animals perinatally exposed: THC-exposed females exhibit a clear increase of this adrenal hormone, whereas THC-exposed males displayed lower levels of this hormone.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…A second phase of inhibition and/or adaptation may follow, with functional resumption (tendency to hyperactivity) during rest, until the response capacities are exhausted due to repetition of the stimulus (Smookler and Buckleyet, 1969;Mallion, 1974;Softowa, 1983;Axelsson and Lindgren, 1985;Dengerink et al, 1985;Colletti, 1985;Gue et al, 1987;Manninen, 1988;Theorell, 1990;Gamallo et al, 1992;Carter et al, 1994;Tomei et al, 1998).…”

Section: Introductionmentioning

confidence: 97%

Acute experimental exposure to noise and hormonal modifications

Tomei¹,

Ruffino

Tomao³

et al. 2000

Journal of Environmental Science and Health, Part A

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The purpose of this study was to analyse, in healthy volunteers exposed to noise of high intensity, any changes in certain hormonal parameters that might be related to psychological and behavioural effects. The parameters studied were cortisol (CORT), dehydroepiandrosterone-sulphate (DHEA-S), prolactin (PRL), growth hormone (GH), insulin (IRI). Some subjective spontaneously expressed parameters, such as feeling cold, feeling sleepy, being bothered by noise and feeling uneasy, feeling nausea, were also taken into consideration. A significant reduction of cortisol compared to the base values was noted both during exposure to noise and at the end of the stimulus. The DHEA-S values increased compared to the base values during administration of the noise and after exposure had finished. After the end of the noise stimulus, prolactin showed a reduction compared to pre-and post-exposure values. Compared to the basic values, GH diminished both during and after exposure to noise. Insulinaemia showed a significant increase of the value during exposure to noise, both compared with 537

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Acute noise stress, ACTH administration, and blood pressure alteration

Cited by 16 publications

References 42 publications

Adrenal toxicology: a strategy for assessment of functional toxicity to the adrenal cortex and steroidogenesis

Adrenal toxicology: a strategy for assessment of functional toxicity to the adrenal cortex and steroidogenesis

Sex-dimorphic psychomotor activation after perinatal exposure to (−)-Δ9-tetrahydrocannabinol. An ontogenic study in wistar rats

Acute experimental exposure to noise and hormonal modifications

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