Tissue Hormone Levels Research Articles

In UteroProgramming of Later Adiposity: The Role of Fetal Growth Restriction

Intrauterine growth restriction (IUGR) is strongly associated with obesity in adult life. The mechanisms contributing to the onset of IUGR-associated adult obesity have been studied in animal models and humans, where changes in fetal adipose tissue development, hormone levels and epigenome have been identified as principal areas of alteration leading to later life obesity. Following an adverse in utero development, IUGR fetuses display increased lipogenic and adipogenic capacity in adipocytes, hypoleptinemia, altered glucocorticoid signalling, and chromatin remodelling, which subsequently all contribute to an increased later life obesity risk. Data suggest that many of these changes result from an enhanced activity of the adipose master transcription factor regulator, peroxisome proliferator-activated receptor-γ (PPARγ) and its coregulators, increased lipogenic fatty acid synthase (FAS) expression and activity, and upregulation of glycolysis in fetal adipose tissue. Increased expression of fetal hypothalamic neuropeptide Y (NPY), altered hypothalamic leptin receptor expression and partitioning, reduced adipose noradrenergic sympathetic innervations, enhanced adipose glucocorticoid action, and modifications in methylation status in the promoter of hepatic and adipose adipogenic and lipogenic genes in the fetus also contribute to obesity following IUGR. Therefore, interventions that inhibit these fetal developmental changes will be beneficial for modulation of adult body fat accumulation.

Effects of thyroxine administration on the growth and survival of pike silverside (Chirostoma estor) juveniles

The pike silverside has high aquaculture potential despite its slow growth. In this study, thyroxine (T4) concentrations (0.13, 1.3 and 13 nM), a control with no hormonal supplement and a negative control containing 4.5 mM methimazole (MMI) were tested to evaluate the growth of this species. Juveniles (0.2 g) were exposed by immersion to these treatments for 8 h every second day for 120 days, and growth evaluations were performed monthly over the entire trial period. In addition, tissue samples from each treatment group were assayed for triiodothyronine (T3) and deiodinase type 2 (D2) activity . The survival rates in all T4 groups were high, and a significant increase in growth was observed (average of 58%). The MMI treatment caused an increase in mortality and a reduction in the final body weight compared with the control. T4 administration did not affect the tissue levels of T3, and it decreased muscular D2 activity only after 30 days of exposure. These results demonstrated that low concentrations of T4 in the culture environment could improve the growth of this species without affecting tissue hormone levels. The technique may have useful applications for early-stage aquaculture of this and other economically important species.

Thyroid Replacement Therapy and Heart Failure

Heart failure (HF) is a major public health and economic problem in Western countries and is one of the most common causes of hospitalization and death. Coronary artery disease is the underlying cause in more than two thirds of chronic HF patients. By 2020, the World Health Organization projects that ischemic heart disease alone will be the most important global cause of morbidity and mortality. The estimated increases in HF-related morbidity and mortality suggest that our understanding of the pathophysiological mechanisms of this syndrome is inadequate. Interest in the role of thyroid hormones (THs) in HF has increased in recent years. The driving considerations can be summarized as follows: (1) the known effects of THs on contractile and relaxation properties of the heart; (2) experimental findings offering strong support for the hypothesis that TH signaling is critical in preserving cardiac structure and performance under normal conditions and after cardiac injury; and (3) evidence that mildly altered TH function is strongly associated with a worsening prognosis in cardiac patients in general and in HF patients in particular. Diastolic function and systolic function are clearly influenced by THs.1 Ventricular contractile function is also influenced by changes in hemodynamic conditions secondary to TH effects on peripheral vascular tone.1 TH homeostasis preserves positive ventricular-arterial coupling, leading to a favorable balance for cardiac work. A study in rats demonstrated that chronic hypothyroidism alone can eventually lead to HF.2 Other studies suggest reduced cardiac tissue triiodothyronine (T3) levels after myocardial infarction (MI) or with development of hypertension by upregulating type 3 deiodinase (D3), which leads to deactivation of T3 and T4 (thyroxine).3–6 This review highlights a growing body of evidence from animal studies and small-scale clinical trials suggesting that low cellular thyroid activity at the cardiac tissue level may adversely affect HF …

Blood flow in renal tissue, blood pressure, and blood hormone levels in rats with adenine-induced renal failure.

Blood flow in renal tissue, blood pressure, and blood hormone levels in rats with adenine-induced renal failure.

Functional Effects of Short-Term Treatment with Amiodarone on Thyroid Tissues of the Rabbit

The effect of short-term treatment with Amiodarone on thyroid gland tissue was studied in a group of 26 New Zealand albino rabbits. Ten rabbits were left untreated and served as controls; the remaining animals were treated with 10 mg/kg/day Amiodarone. The serum levels of serum triiodothyronine (T3), thyroxine (T4), and thyroid stimulating hormone (TSH) levels were measured at days 0 (baseline), 7, 30, and 45. The serum selenium levels were also measured, but only on days 0 and 45 of the experiment. At the end of the experiment the animals were sacrificed and the levels of selenium, T3, T4, and iodine were determined in thyroid tissue. After 30 days treatment the values of T3 were significantly lower than those of the untreated controls or the baseline levels (p < 0.001). The T4 level was significantly lower and the TSH value was significantly higher after 45 days of Amiodarone (p < 0.001). In thyroid tissue the T3, T4, and iodine levels were significantly higher in the treated group when compared to untreated controls (p < 0.05). These results show that Amiodarone induces changes in the hormone levels in both serum and thyroid tissues, as well as in the amount of iodine taken up by the thyroid gland in rabbits.

Does testosterone administration affect the prostate?

Millions of men are candidates for testosterone replacement therapy (TRT), but a major safety concern, the effects of TRT on the prostate, has been poorly understood until recently. In the past few years, a meta-analysis showed that endogenous hormone levels have little relationship to prostate cancer. Another review showed that during TRT, cancer develops with no more frequency than in the overall population. A randomized trial focusing on TRT’s tissue effects showed that no treatment-related change was noted in prostate tissue composition, hormone levels, biomarkers, gene expression, or cancer incidence. And in animal models, testosterone alone is at most only a weak prostatic carcinogen. Thus, recent years have seen clarification of the prostate safety issue. Future areas of interest include using TRT in men believed to be cured of prostate cancer and, importantly, developing cancer-specific biomarkers (eg, PCA3 gene) to help diagnose and monitor men receiving TRT.

The efficacy of alum-containing ferrous thermal water in the management of chronic inflammatory gynaecological disorders—A randomized controlled study

Objectives Treatment of gynaecological disorders is a frequent, but only barely substantiated application of balneotherapy. This study investigated potential differences between the clinical symptoms, pelvic blood flow and specific laboratory parameters of patients undergoing balneotherapy with two different types of immersion: alum-containing and tap water. Study design The study population comprised 40 patients (mean age: 39.4 years), randomized into two groups. All subjects took 20 min baths in 38 °C water every other day, for 10 occasions altogether. Study parameters were: pain relief, reduction in tissue growth, hormone levels, psychic status, and pelvic blood flow. Results Thermal water improved the clinical parameters of both groups significantly. In comparison with tap water, treatment with alum-containing water accomplished significantly greater progress, as reflected by the relief of pain elicited by handling the uterus and improvement of psychic status. Laboratory parameters (FSH, LH, prolactin, oestradiol and beta-endorphin serum levels) and the Doppler index did not change in either group. Conclusions As demonstrated by our results, 3-week balneotherapy is a potentially useful adjunct for the management of chronic pelvic inflammatory disease, but further, long-term studies are notwithstanding necessary.

Acylation-stimulating protein/C5L2-neutralizing antibodies alter triglyceride metabolism in vitro and in vivo

Acylation-stimulating protein (ASP), a lipogenic hormone, stimulates triglyceride (TG) synthesis and glucose transport upon activation of C5L2, a G protein-coupled receptor. ASP-deficient mice have reduced adipose tissue mass due to increased energy expenditure despite increased food intake. The objective of this study was to evaluate the blocking of ASP-C5L2 interaction via neutralizing antibodies (anti-ASP and anti-C5L2-L1 against C5L2 extracellular loop 1). In vitro, anti-ASP and anti-C5L2-L1 blocked ASP binding to C5L2 and efficiently inhibited ASP stimulation of TG synthesis and glucose transport. In vivo, neither anti-ASP nor anti-C5L2-L1 altered body weight, adipose tissue mass, food intake, or hormone levels (insulin, leptin, and adiponectin), but they did induce a significant delay in TG clearance [P < 0.0001, 2-way repeated-measures (RM) ANOVA] and NEFA clearance (P < 0.0001, 2-way RM ANOVA) after a fat load. After treatment with either anti-ASP or anti-C5L2-L1 antibody there was no change in adipose tissue AMPK activity, but neutralizing antibodies decreased perirenal TG mass (-38.4% anti-ASP, -18.8% anti-C5L2, P < 0.01-0.001) and perirenal LPL activity (-75.6% anti-ASP, -72.5% anti-C5L2, P < 0.05). In liver, anti-C5L2-L1 decreased TG mass (-42.8%, P < 0.05), whereas anti-ASP increased AMPK activity (+34.6%, P < 0.001). In the muscle, anti-C5L2-L1 significantly increased TG mass (+128.0%, P < 0.05), LPL activity (+226.1%, P < 0.001), and AMPK activity (+71.1%, P < 0.01). In addition, anti-ASP increased LPL activity (+164.4, P < 0.05) and AMPK activity (+53.9%, P < 0.05) in muscle. ASP/C5L2-neutralizing antibodies effectively block ASP-C5L2 interaction, altering lipid distribution and energy utilization.

Persistent Intraprostatic Androgen Concentrations after Medical Castration in Healthy Men

The impact of serum androgen manipulation on prostate tissue hormone levels in normal men is unknown. Studies of men with prostate cancer have suggested that prostatic androgens are preserved in the setting of castration. Tissue androgens might stimulate prostate growth, producing adverse clinical consequences. The objective of the study was to determine the effect of serum androgen manipulation on intraprostatic androgens in normal men. Thirteen male volunteers ages 35-55 yr (prostate-specific antigen < 2.0 ng/ml; normal transrectal ultrasound) were randomly assigned to: 1) a long-acting GnRH-antagonist, acyline, every 2 wk; 2) acyline plus testosterone (T) gel (10 mg/d); or 3) placebo for 28 d. Serum hormones were assessed weekly. Prostate biopsies were obtained on d 28. Extracted androgens were measured by RIA, and immunohistochemistry for androgen-regulated proteins was performed. The mean decrease in serum T was 94%, whereas prostatic T and dihydrotestosterone levels were 70 and 80% lower, respectively, in subjects receiving acyline alone compared with controls (P < 0.05). Despite this decrease in prostate androgens, there were no detectable differences in prostate epithelial proliferation, apoptosis, prostate-specific antigen, and androgen receptor expression. In this small study of healthy subjects, despite a 94% decrease in serum T with medical castration, intraprostatic T and dihydrotestosterone levels remained 20-30% of control values, and prostate cell proliferation, apoptosis, and androgen-regulated protein expression were unaffected. Our data highlight the importance of assessing tissue hormone levels. The source of persistent prostate androgens associated with medical castration and their potential role in supporting prostate metabolism deserves further study.

Dementia and Testosterone Levels in Men

To the Editor: The study by Ms Rosario and colleagues reports a relationship between low postmortem brain testosterone levels and preceding dementia in men. To be able to interpret these data it would have been valuable to know the potential impact on their results of body mass index, the intensity of care over the interval immediately preceding death, and recent opioid use. Obesity is associated with diminished serum testosterone and elevated serum estradiol. Expectant care, with no therapeutic interventions for several days immediately preceding death, may have modified tissue hormone levels in comparison with the levels of patients dying while undergoing active therapy. Opioid-induced androgen deficiency usually develops within a few hours of administration of relatively small doses of opioid medications, with plasma testosterone levels occasionally reaching near-castrate range within 24 hours. These low levels are maintained during continued opioid administration. Although tissue concentrations of sex hormones have not been measured during opioid use, the frequent use of these medications during end-of-life patient managementsuggests that theiradministrationshouldbeconsidered in interpreting postmortem tissue sex hormone levels. In contrast to levelsof testosterone,opioid-induced loweringofserum estradiol develops much more slowly, a difference that could have contributed to the observations reported.

Cloning and characterization of human form 2 type 7 17β-hydroxysteroid dehydrogenase, a primarily 3β-keto reductase and estrogen activating and androgen inactivating enzyme

Type 7 17β-HSD catalyzes the transformation of estrone (E1) into estradiol (E2) and dihydrotestosterone (DHT) into 5α -androstane-3β,17β-diol (3β-diol) as well as zymosterone into zymosterol. This suggests that in addition to cholesterol metabolism, the enzyme could play a critical role in estrogen-sensitive cells, since it inactivates DHT that generally shows antagonistic effect in the cells, while producing active E2 for cell proliferation. In this report, we describe the cloning and characterization of a second form of type 7 17β-HSD (17β-HSD7_2) that shares 95.6% identity with 17β-HSD7_1. Using a 7.5 kb genomic DNA fragment of 17β-HSD7_1 as probe, we have obtained 7 BAC clones: three clones containing the 17β-HSD7_1 gene and four containing the 17β-HSD7_2 gene. The corresponding 17β-HSD7_2 cDNA fragments of the coding region were obtained by amplification using RT-PCR and subcloned into pCMV expression vector and stably transfected into human embryonic kidney (HEK-293) cells. The overexpressed 17β-HSD7_2 catalyzes efficiently the transformation of E1 into E2 and of DHT into 3β-diol. Ribonuclease protection assays (RPA) indicate that 17β-HSD7_2 is expressed in the liver, prostate, uterus and placenta. FISH mapping using the 7.5 kb genomic DNA fragment as well as 2 BAC clones of each form allowed us to map the 17β-HSD7_1 gene on chromosome band 1q23, and 17β-HSD7_2 on band 10p11.2. These results contrast with a previous report that the 17β-HSD7_1 gene was mapped to chromosomal band 10p11.2. This newly identified form of 17β-HSD7 could have a significant role by modulating active hormone levels in estrogen-sensitive cells or tissues.

Maternity and bone mineral density

During pregnancy and lactation, changes occur in a variety of factors which have great potential to influence bone mineral density (BMD). Smoking habits, the level of alcohol consumption, the level of physical activity, body weight, soft tissue composition and hormone levels are all factors that change during the course of these conditions. Some of these factors are capable of increasing BMD, and some can reduce it. Due to these various changes, it is virtually impossible to predict the development in BMD that will occur during a pregnancy and lactation. However, longitudinal studies have suggested that both pregnancy and lactation are associated with a BMD loss of up to 5%, albeit that the BMD recovers after weaning. Cross-sectional studies have indicated that women with many children and a long total period of lactation have similar or higher BMD and similar or lower fracture risk than their peers who have not given birth. As the studies showing this trend have been observational and cross-sectional case-control studies, the conclusions can only be regarded as being suggestive, and no causality can be proven.

Effects of Anoectochilus formosanus Hayata extract and glucocorticoid on lung maturation in preterm rats

We investigated the effects of maternal administration of Anoectochilus formosanus extract and dexamethasone on lung maturation in preterm rats. A. formosanus group mothers were tube-fed A. formosanus extract (300 mg/kg body wt./day) for 7 days from days 12-18 of gestation. Dexamethasone group mothers were injected intraperitoneally with dexamethasone (0.2 mg/kg body wt.) in saline on day 18 of gestation. Control group mothers were similarly injected with saline alone. On day 19 of gestation, fetuses were delivered by cesarean section. A. formosanus treatment significantly increased the fetal lung/body weight ratio, as compared to dexamethasone treatment. Saturated phosphatidylcholine levels in fetal lung tissue and growth hormone levels in maternal serum were significantly increased in the A. formosanus- and dexamethasone-treated groups as compared to controls. The histological appearance of preterm rat lungs revealed extensive branching of intermediate airways, denser mesenchyme, and more epithelial tubules in the dexamethasone and A. formosanus groups as compared with the control group. These results suggest that antenatal A. formosanus treatment may play a role in accelerating fetal rat lung maturation.

The pattern of estradiol and progesterone differs in serum and tissue of benign and malignant ovarian tumors

Epidemiological studies have indicated a relationship between gonadal steroid hormones and ovarian cancer. A production of both estradiol and progesterone by ovarian cancers has been demonstrated. The local steroid concentrations and the putative relation to histopathological and clinical condition were investigated herein. Ovarian tissue, ovarian tumor cyst fluid, ovarian vein samples and peripheral serum concentrations of estradiol and progesterone in pre- and post-menopausal women, subdivided into groups with normal ovaries, benign, borderline and malignant ovarian tumors, were quantitatively assessed. Both ovarian tissue concentrations of estradiol and progesterone were more than 100-fold higher than in serum. Based on differences in concentrations between different ovarian tumor groups, the data is not coherent with the previously suggested increased production of estradiol and progesterone in ovarian cancer tissue, since post-menopausal women with ovarian cancer presented lower median tissue hormone levels, most pronounced between malignant and benign tumors; median (25 and 75 percentile) estradiol; 9.40 (6.67-15.50) vs 16.44 (12.49-23.20), p=0.02 and progesterone; 308 (240-575) vs 957 (553-1143) pmol/g wet weight, p<0.01, n=81. Lower concentrations of estradiol, but not progesterone, were found in ovarian cancer tissue, ovarian cyst fluid and peripheral serum in patients with FIGO stages 3 and 4 than in stages 1 and 2. The novel finding of a large ovarian tissue to serum difference of both estradiol and progesterone indicates an important role of ovarian tissue concentrations in tumor biology and raises the question of adequate doses of anti-hormonal therapy in women with ovarian cancer.

Thyroid of Lake Sturgeon, Acipenser fulvescens: I. Hormone Levels in Blood and Tissues

The authors measured thyroid hormone (TH) levels in plasma, whole carcass, and tissues of cultured 2-year-old immature lake sturgeon held in fresh water and in serum of adults at spawning time from the Winnipeg River. Circulating thyroxine (T4) and 3,5,3′-triiodothyronine (T3) levels were low (T4 ∼ 0.3 ng/ml, T3 ∼ 0.2 ng/ml) in all cultured fish and most adults, but a few of the latter had exceptionally high T4 and T3 levels. The percentages of blood TH found in erythrocytes were 19.5% (T4), 6.1% (T3) and 6.9% (reverse T3 = rT3). Equilibrium dialysis showed much higher percentages of plasma free (F) FT4 (1.1%), FT3 (0.4%), and FrT3 (3,3′,5′-triiodothyronine = rT3, 3.0%) for sturgeon than for rainbow trout, indicating more limited TH binding to sturgeon plasma sites. However, concentrations of FT4 and FT3 were close to those reported for salmonids. T3 levels exceeded T4 levels in most extrathyroidal tissues of cultured sturgeon but in most cases were less than 0.1 ng/g and 10 to 100 times lower than reported for salmonids; only the whole brain T3 concentration (5.6 ng/g) approached that of salmonids. The digested thyroid contained 21.3 ng T3/g and 2.4 ng T4/g. The authors conclude that lake sturgeon have a low circulating reserve of bound TH but have FT4 and FT3 concentrations close to those of salmonids. The high thyroidal T3:T4 ratio and low tissue T4 levels suggest that, in contrast to teleosts studied to date, the thyroid may be a significant direct source of T3, the primary TH in sturgeon tissues. High serum T4 and T3 levels in some sturgeon at spawning time may suggest a thyroid role in reproduction.

Biochemical and histopathological effects of carbendazim to rat male reproduction

The purpose of this study was to determine the effects of carbendazim (methyl 2-benzimidazole carbamate) on the some hormone levels and on testis tissue. Carbendazim in the doses of 0, 150, 300, and 600 mg/kg/day were administered (by gavage) to male rats, daily for 15 weeks. At the end of the experiment serum total testosterone and dihydrotestosterone (DHT) levels were analyzed and testis tissues were taken for light and electron microscopic examinations. A statistically significant decrease in total serum testosterone level in rats exposed to carbendazim (dose: 300 and 600 mg/kg/day), compared to the control, was observed. Also, dihydrotestosterone level was significantly decreased in all experimental groups. Histopathologically, carbendazim caused detrimental effects in testis tissues. These effects were vacuolization, disorganization and necrosis in germinal epithelium. In addition, multinucleated giant cells were observed in the lumen of the seminiferous tubules. These pathological findings were supported by electron microscopic examinations. These results suggest that carbendazim, in subchronic exposure, affects testis tissue and androgenic hormone levels.

Development of a human stanniocalcin radioimmunoassay: serum and tissue hormone levels and pharmacokinetics in the rat

Stanniocalcin (STC) is a polypeptide hormone that was first discovered in fish and recently identified in humans and other mammals. In fish STC is produced by one gland, circulates freely in the blood and plays an integral role in mineral homeostasis. In mammals, STC is produced in a number of different tissues and serves a variety of different functions. In kidney, STC regulates phosphate reabsorption by proximal tubule cells, whereas in ovary it appears to be involved in steroid hormone synthesis. However there is no information on circulating levels of STC in mammals or the regulation of its secretion. In this report we have developed a radioimmunoassay (RIA) for human STC. The RIA was validated for measuring tissue hormone levels. However human and other mammalian sera were completely devoid of immunoreactive STC (irSTC). To explore the possibility that mammalian STC might have a short half-life pharmacokinetic analysis was carried out in rats. STC pharmacokinetics were best described by a two compartment model where the distribution phase (t1/2 α) equaled 1 min and the elimination phase (t1/2 β) was 60 min. However the STC in the elimination phase no longer crossreacted in the RIA indicating it had undergone substantial chemical modification, which could explain our inability to detect irSTC in mammalian sera. When we compared the pharmacokinetics of human and fish STC in mammalian and fish models the human hormone was always eliminated faster, indicating that human STC has unique structural properties. There also appears to be a unique clearance mechanism for STC in mammals. Hence there are major differences in the delivery and biology of mammalian STC. Unlike fishes, mammalian STC does not normally circulate in the blood and functions instead as a local mediator of cell function. Future studies will no doubt show that this has had important ramifications on function as well.

Serum and tissue hormone levels of vaginally and orally administered estradiol

Objective: Our purpose was to determine serum and endometrial estradiol levels when micronized estradiol is administered vaginally and orally. Study Design: Five subjects were given oral estradiol (2 mg twice daily), during an artificial luteal phase, and another group of 5 subjects were given the same dose of estradiol by the vaginal route. Endometrial biopsies and blood samples were obtained on day 21 of the cycle, 2 hours after the last dose was administered. Tissue and blood samples were assayed for estradiol. Results: Serum estradiol levels were significantly higher with vaginally administered estradiol than with orally administered estradiol (2344 ± 398 vs 279 ± 76 pg/mL, P < .005). Endometrial estradiol concentrations were also significantly higher with vaginally administered estradiol than with the oral preparation (918 ± 412 vs 13 ± 2 pg/mg protein, P < .05). Conclusions: Vaginal administration of estradiol is more effective in increasing serum and endometrial levels of estradiol than the oral route and may represent the optimal route of administration for recipients of egg donation. If the vaginal route of estradiol administration is considered for menopausal replacement therapy, much lower doses of the standard oral quantities should be used. Furthermore, if the uterus is present, a progestin must be used to compensate for the high tissue levels of estradiol. (Am J Obstet Gynecol 1999;180:1480-3.)

Regulation of expression of the rodent cytosolic sulfotransferases.

Understanding the molecular regulation of the sulfotransferases is important because these enzymes are essential to a number of critical biological processes. Sulfotransferase expression clearly plays a role in xenobiotic detoxication, carcinogen activation, prodrug processing, cellular signaling pathways, and the regulation of intratissue active androgen and estrogen levels. Although cytosolic sulfotransferases are present in the gut, adrenal, kidney, lung, skin, brain, and other extrahepatic tissues, the basis for the molecular regulation of this complicated gene family has been best characterized in the rat liver, where sulfotransferase levels are relatively abundant. Advances in genomic cloning and in the molecular characterization of individual sulfotransferase cDNAs have inspired new insights into the mechanisms involved in sulfotransferase gene regulation. In particular, the hypothalamic-pituitary-gonadal-adrenocortical axis appears to play a significant role in the regulation of individual sulfotransferase genes. The molecular signals that fluctuate with developmental age, gender, and the occurrence of systemic endocrinopathies also influence sulfotransferase gene expression. For example, diabetes, which disrupts glucose and ketone homeostasis, insulin sensitivity, gonadal and neuroendocrine hormone balance, protein kinase C isoform expression, and P450 metabolism, also disturbs hepatic sulfotransferase gene expression. What role does sulfotransferase expression play in target organ toxicity? Do xenobiotic-mediated changes in sulfotransferase expression compromise detoxication? Does deregulated sulfotransferase expression during development lead to birth defects by perturbing the delicate balance of active hormone levels in fetal tissues? Do conditions of glucocorticoid excess, such as stress or high-dose glucocorticoid therapy induce sulfotransferase expression and place toxicant and carcinogen bioactivation systems in overdrive? This review will summarize our current understanding of the molecular and cellular regulation of the major rodent cytosolic sulfotransferases. Only by thoroughly dissecting the regulation of this important multigene family in rodent liver, where sulfotransferase expression is most abundant, can we begin to focus on more pressing questions concerning the role of the sulfotransferases in the genesis of endocrinopathies and cancer in humans.

The Physiological Role of Abscisic Acid in Eliciting Turion Morphogenesis.

The exogenous application of hormones has led to their implication in a number of processes within the plant. However, proof of their function in vivo depends on quantitative data demonstrating that the exogenous concentration used to elicit a response leads to tissue hormone levels within the physiological range. Such proof is often lacking in many investigations. We are using abscisic acid (ABA)-induced turion formation in Spirodela polyrrhiza L. to investigate the mechanism by which a hormone can trigger a morphogenic switch. In this paper, we demonstrate that the exogenous concentration of ABA used to induce turions leads to tissue concentrations of ABA within the physiological range, as quantified by both enzyme-linked immunosorbent assay and high-performance liquid chromatography/gas chromatography-electron capture detection analysis. These results are consistent with ABA having a physiological role in turion formation, and they provide an estimate of the changes in endogenous ABA concentration required if environmental effectors of turion formation (e.g. nitrate deficiency, cold) act via an increased level of ABA. In addition, we show that the (+)- and (-)-enantiomers of ABA are equally effective in inducing turions. Moreover, comparison of the ABA; levels attained after treatment with (+)-, (-)-, and ([plus or minus])-ABA and their effect on turion induction and comparison of the effectiveness of ABA on turion induction under different pH regimes suggest that ABA most likely interacts with a plasmalemma-located receptor system to induce turion formation.