Risk assessment of ionizing radiation and radiological thresholds to compound an environmental baseline for the unconventional gas industry.

The exploration of unconventional hydrocarbons may be very effective in promoting economic development and confronting energy crisis around the world. However, the environmental risks associated with this practice might be an impediment if not adequately dimensioned. In this context, naturally occurring radioactive materials and ionizing radiation are sensitive aspects in the unconventional gas industry that may compromise the environmental sustainability of gas production and they should be properly monitored. This paper provides a radioecological assessment of the São Francisco Basin (Brazil) as part of an environmental baseline evaluation regarding the Brazilian potential for exploring its unconventional gas reserves. Eleven and thirteen samples of surface waters and groundwater were analyzed for gross alpha and beta using a gas flow proportional counter. A radiological background range was proposed using the ± 2 Median Absolute Deviation method. Using geoprocessing tools, the annual equivalent doses and lifetime cancer risk indexes were spatialized. Gross alpha and beta background thresholds in surface water ranged from 0.04-0.40 Bq L-1 to 0.17-0.46 Bq L-, respectively. Groundwater radiological background varies from 0.006-0.81 Bq L-1 to 0.06-0.72 Bq L-1 for gross alpha and beta, respectively. All environmental indexes are relatively higher in the south of the basin, probably a direct response to the local volcanic formations. Traçadal fault and local gas seepages might also influence the gross alpha and beta distribution. All samples have radiological indexes below the environmental thresholds, and should remain at acceptable levels with the development of the unconventional gas industry in Brazil.

Mandible analysis in sex steroid-deficient rats.

The aim of this study was to evaluate, by morphologic techniques, the effects of sex steroid deficiency on mandible bone remodeling of female rats, in groups of different experimental periods and to compare the results with 90-day orquiectomized males. Female and male Wistar rats, 3 months old, were divided into experimental groups and at the end of each experimental period were killed, and mandibles were extracted. The left mandibles were prepared with rote technique bone and examined by a light microscope. Morphological analyses of the mandibles demonstrated resorption signals in the alveolar bone, after 30 days in ovariectomized females, but it was more intense 90 days after castration. The orquiectomized group exhibited some signals of resorption similar to the ovariectomized group of 60 days. Morphometric analysis of alveolar bone thickness in females after 60 days was in agreement with morphological results. However, the analysis of periodontal ligament thickness did not show any significant difference. There were variations in sexual hormone deficiency in the mandibles of males and females and they seemed to be more precocious in ovariectomized than in orquiectomized rats. It is important for a health professional to have knowledge about bone metabolism to improve the quality of life of postmenopaused and old people.

Sex steroids modulate rat anterior pituitary and liver iodothyronine deiodinase activities.

In this study, we investigated the sex hormone regulation of 5'-iodothyronine deiodinase activity, which is responsible for enzymatic conversion of thyroxine into the bioactive form, triiodothyronine. Pituitary homogenates and liver microsomes from: 1) ovariectomized rats injected with 17-beta-estradiol benzoate and/or progesterone (0.7 and 250 microg/100 g body weight, respectively, subcutaneously, over 10 days); 2) male castrated rats treated or not with 0.4 mg/100 g body weight testosterone propionate, intramuscular, over 7 days, were assayed for type 1 and type 2 deiodinase activity in the pituitary. Enzyme activities were measured by release of (125)I from deiodination of (125)I reverse triiodothyronine under varying assay conditions. Estrogen stimulated anterior pituitary and liver type 1 deiodinase activity in ovariectomized rats (45 and 30 %, p < 0.05). Progesterone inhibited the liver enzyme (40 %, p < 0.05), and had no effect on the pituitary, but in both tissues, blocked estrogen stimulatory effect on type 1 deiodinase. In males, testosterone normalized the reduced liver type 1 deiodinase of castrated rats. However, in the pituitary, castration increased (50 %) type 1 deiodinase independent of testosterone treatment, suggesting the existence of a inhibitory testicular regulator of pituitary type 1 enzyme. Treatments did not alter pituitary type 2 deiodinase activity. In conclusion, gonads and sex steroids differentially modulate type 1 deiodinase activity in rat pituitary and liver.

Chlorophyll-a determination via continuous measurement of plankton fluorescence: methodology development.

A methodology is presented for the continuous measurement of chlorophyll-a concentration due to plankton, in surface water environments. A Turner 10-AU fluorometer equipped with the F4T5.B2/BP lamp (blue lamp), a Cs 5-60 equivalent excitation path filter, and a 680 nm emission filter, has been used. This configuration allows the in vivo, in situ determination of chlorophyll-a by measuring the fluorescence due to the pigments. In field work the fluorometer, data logging and positioning equipment were placed aboard a manageable boat which navigated following a scheme of regularly spaced crossings. Some water samples were collected during the measurement for laboratory chlorophyll-a measurements by the spectrophotometric method, thus providing for calibration and comparison. Spatial chlorophyll-a concentration distributions can be easily defined in large volumes, such as reservoirs, etc. Two distinct environments have been monitored: in the Vargem das Flores reservoir chlorophyll-a concentrations varied between 0.7 and 2.6 mg/m3, whereas in the Lagoa Santa lake these values lied in the 12 to 18 mg/m3 range. The simplicity, versatility and economy of the method, added to the large amount of data that can be gathered in a single run, clearly justify its use in field environmental studies.

Acrosomal ultrastructure of stallion spermatozoa cryopreserved with ethylene glycol using two packaging systems.

The present experiments aimed to examine the substitution of glycerol (G) by ethylene glycol (E) as a cryoprotective agent for stallion spermatozoa. Two different ethylene glycol concentrations (5% and 10%) and also the association of glycerol (2%) and ethylene glycol (3%) (E/G) were studied (Experiment 1). In Experiment 2, two packing systems (0.5 x 4.0 ml) were evaluated using both cryoprotectors. In both experiments, the sperm membrane integrity after freezing was evaluated using transmission electron microscopy. The mean post-thaw motility was 34.25, 36.5, 29.25 and 34.75% for G5%, E5%, E10% and E/G, respectively. It was observed that the percentage of motile spermatozoa was significantly smaller (P<0.05) when semen was processed with E10%. A decrease in the acrosome integrity was observed in frozen thawed spermatozoa from all treated groups. It was observed that 28.0, 22.5, 25.5 and 22.5% of the sperm cells had a normal acrosome following freezing with G5%, E5%, E10% and E/G, respectively. Undulation of the outer acrosomal membrane, acrosomal swelling and loss of acrosomal content density and homogeneity were the most evident ultrastructural alterations observed. In Experiment 2, the post-thaw motility was higher (P<0.05) for sperm frozen in 0.5 ml straws than in 4.0 ml straws, regardless of the cryoprotector used. The ultrastructural evaluation showed 26.7 and 16.0% of intact acrosomes for sperm frozen in 0.5 ml and 4.0 ml straws, respectively. We concluded that ethylene glycol has similar cryoprotective properties to glycerol and that utilisation of 0.5 ml straws improved the ability of horse sperm cells to withstand damage after the cryopreservation process.

Effect of medroxyprogesterone acetate on thyrotropin secretion in adult and old female rats.

Steroid hormones have been implicated in the modulation of TSH secretion; however, there are few and controversial data regarding the effect of progesterone (Pg) on TSH secretion. Medroxyprogesterone acetate (MPA) is a synthetic alpha-hydroxyprogesterone analog that has been extensively employed in therapeutics for its Pg-like actions, but that also has some glucocorticoid and androgen activity. Both hormones have been shown to interfere with TSH secretion. The objective of the present study was to investigate the effects of MPA or Pg administration to ovariectomized (OVX) rats on in vivo and in vitro TSH release and pituitary TSH content. The treatment of adult OVX rats with MPA (0. 25 mg/100 g body weight, sc, daily for 9 days) induced a significant (P<0.05) increase in the pituitary TSH content, which was not observed when the same treatment was used with a 10 times higher MPA dose or with Pg doses similar to those of MPA. Serum TSH was similar for all groups. MPA administered to OVX rats at the lower dose also had a stimulatory effect on the in vitro basal and TRH-induced TSH release. The in vitro basal and TRH-stimulated TSH release was not significantly affected by Pg treatment. Conversely, MPA had no effect on old OVX rats. However, in these old rats, ovariectomy alone significantly reduced (P<0.05) basal and TRH-stimulated TSH release in vitro, as well as pituitary TSH content. The results suggest that in adult, but not in old OVX rats, MPA but not Pg has a stimulatory effect on TSH stores and on the response to TRH in vitro.

Effect of medroxyprogesterone acetate on thyrotropin secretion in adult and old female rats

Steroid hormones have been implicated in the modulation of TSH secretion; however, there are few and controversial data regarding the effect of progesterone (Pg) on TSH secretion. Medroxyprogesterone acetate (MPA) is a synthetic alpha-hydroxyprogesterone analog that has been extensively employed in therapeutics for its Pg-like actions, but that also has some glucocorticoid and androgen activity. Both hormones have been shown to interfere with TSH secretion. The objective of the present study was to investigate the effects of MPA or Pg administration to ovariectomized (OVX) rats on in vivo and in vitro TSH release and pituitary TSH content. The treatment of adult OVX rats with MPA (0.25 mg/100 g body weight, sc, daily for 9 days) induced a significant (P<0.05) increase in the pituitary TSH content, which was not observed when the same treatment was used with a 10 times higher MPA dose or with Pg doses similar to those of MPA. Serum TSH was similar for all groups. MPA administered to OVX rats at the lower dose also had a stimulatory effect on the in vitro basal and TRH-induced TSH release. The in vitro basal and TRH-stimulated TSH release was not significantly affected by Pg treatment. Conversely, MPA had no effect on old OVX rats. However, in these old rats, ovariectomy alone significantly reduced (P<0.05) basal and TRH-stimulated TSH release in vitro, as well as pituitary TSH content. The results suggest that in adult, but not in old OVX rats, MPA but not Pg has a stimulatory effect on TSH stores and on the response to TRH in vitro

[Compliance in antihypertensive therapy: analyses in scientific articles]. / A adesão ao tratamento na hipertensão arterial: análise da produção científica.

The aim of this study was to evaluate scientific articles published between 1991-1995, in order to identify the compliance in antihypertensive therapy, One hundred seven scientific articles were evaluated. The results showed that 68% were related to patient, 63% to pharmacological treatment, 62% general, 39% non pharmacological treatment, 34% organizational factors, and 8% related to disease. Compliance with antihypertensive therapy was the major challenge of hypertension management and to know how this aspect was focalized in scientific articles possible reduce non compliance in hypertension.

Effects of estradiol benzoate on 5'-iodothyronine deiodinase activities in female rat anterior pituitary gland, liver and thyroid gland

There is little information on the possible effects of estrogen on the activity of 5'-deiodinase (5'-ID), an enzyme responsible for the generation of T3, the biologically active thyroid hormone. In the present study, anterior pituitary sonicates or hepatic and thyroid microsomes from ovariectomized (OVX) rats treated or not with estradiol benzoate (EB, 0.7 or 14 mug/100 g body weight, sc, for 10 days) were assayed for type I 5'-ID (5'-ID-I) and type II 5'-ID (5'-ID-II, only in pituitary) activities. The 5'-ID activity was evaluated by the release of (125)I from deiodinated (125)I rT3, using specific assay conditions for type I or type II. Serum TSH and free T3 and free T4 were measured by radioimmunoassay. OVX alone induced a reduction in pituitary 5'-ID-I (control = 723.7 + 67.9 vs OVX = 413.9 + 26.9; P<0.05), while the EB-treated OVX group showed activity similar to that of the normal group. Thyroid 5'-ID-I showed the same pattern of changes, but these changes were not statistically significant. Pituitary and hepatic 5'-ID-II did not show major alterations. The treatment with the higher EB dose (14 mug), contrary to the results obtained with the lower dose, had no effect on the reduced pituitary 5'-ID-I of OVX rats. However, it induced an imporatnt increment of 5'-ID-I in the thyroid gland (0.8 times higher than that of the normal group: control = 131.9 + 23.7 vs OVX + EB 14 mug = 248.0 + 31.2; P<0.05), which is associated with increased serum TSH (0.6-fold vs OVX, P<0.05) but normal serum free T3 and free T4. The data suggest that estrogen is a physiological stimulator of anterior pituitary 5'-ID-I and a potent stimulator of the thyroid enzyme when employed at high doses.

Dose-dependent effects of 17-beta-estradiol on pituitary thyrotropin content and secretion in vitro

We studied the basal and thyrotropin-releasing hormone (TRH) (50 nM) induced thyrotropin (TSH) release in isolated hemipituitaries of ovariectomized rats treated with near-physiological or high doses of 17-Beta-estradiol benzoate (EB; sc, daily for 10 days) or with vehicle (untreated control rats, OVX). One group was sham-operated (normal control). The anterior pituitary glands were incubated in Krebs-Ringer bicarbonate medium, pH 7.4 at 37 C in an atmosphere of 95 percent O2/5 percent CO2. Medium and pituitary TSH was measured by specific RIA (NIDDK-RP-3). Ovariectomy induced a decrease (P<0.05) in basal TSH release (normal control = 44.1 + 7.2; OVX = 14.7 + 3.0 ng/ml) and tendend to reduce TRH-stimulated TSH release (normal control = 33.0 + 8.1; OVX = 16.6 + 2.4 ng/ml). The lowest dose of EB (0.7 mug/100 g body weight) did not reverse this alteration, but markedly increased the pituitary TSH content (0.6 + 0.06 mug/hemipituitary; P<0.05) above that of OVX (0.4 + 0.03 mug/hemipituitary) and normal rats (0.46 + 0.03 mug/hemipituitary). The intermediate EB dose (1.4 mug/100 g body weight) induced a nonsignificant tendency to a higher TSH response to TRH compared to OVX and a lower response compared to normal rats. Conversely, in the rats treated with the highest dose (14 mug/100 g body weight), serum 17-Beta-estradiol was 17 times higher than normal, and the basal and TRH-stimulated TSH release, as well as the pituitary TSH content, was significantly (P<0.05) reduced compared to normal rats and tended to be even lower than the values observed for the vehicle-treated OVX group, suggesting an inhibitory effect of hyperestrogenism. In conclusion, while reinforcing the concept of a positive physiological regulatory role of estradiol on the tSH response to TRH and on the pituitary stores of the hormone, the present results suggest an inhibitory effect of high levels of estrogen on these responses.

Effects of estradiol benzoate on 5'-iodothyronine deiodinase activities in female rat anterior pituitary gland, liver and thyroid gland.

There is little information on the possible effects of estrogen on the activity of 5'-deiodinase (5'-ID), an enzyme responsible for the generation of T3, the biologically active thyroid hormone. In the present study, anterior pituitary sonicates or hepatic and thyroid microsomes from ovariectomized (OVX) rats treated or not with estradiol benzoate (EB, 0.7 or 14 micrograms/100 g body weight, s.c., for 10 days) were assayed for type I 5'-ID (5'-ID-I) and type II 5'-ID (5'-ID-II, only in pituitary) activities. The 5'-ID activity was evaluated by the release of 125I from deiodinated 125I rT3, using specific assay conditions for type I or type II. Serum TSH and free T3 and free T4 were measured by radioimmunoassay. OVX alone induced a reduction in pituitary 5'-ID-I (control = 723.7 +/- 67.9 vs OVX = 413.9 +/- 26.9; P < 0.05), while the EB-treated OVX group showed activity similar to that of the normal group. Thyroid 5'-ID-I showed the same pattern of changes, but these changes were not statistically significant. Pituitary and hepatic 5'-ID-II did not show major alterations. The treatment with the higher EB dose (14 micrograms), contrary to the results obtained with the lower dose, had no effect on the reduced pituitary 5'-ID-I of OVX rats. However, it induced an important increment of 5'-ID-I in the thyroid gland (0.8 times higher than that of the normal group: control = 131.9 +/- 23.7 vs OVX + EB 14 micrograms = 248.0 +/- 31.2; P < 0.05), which is associated with increased serum TSH (0.6-fold vs OVX, P < 0.05) but normal serum free T3 and free T4. The data suggest that estrogen is a physiological stimulator of anterior pituitary 5'-ID-I and a potent stimulator of the thyroid enzyme when employed at high doses.

Dose-dependent effects of 17-beta-estradiol on pituitary thyrotropin content and secretion in vitro.

We studied the basal and thyrotropin-releasing hormone (TRH) (50 nM) induced thyrotropin (TSH) release in isolated hemipituitaries of ovariectomized rats treated with near-physiological or high doses of 17-beta-estradiol benzoate (EB; sc, daily for 10 days) or with vehicle (untreated control rats, OVX). One group was sham-operated (normal control). The anterior pituitary glands were incubated in Krebs-Ringer bicarbonate medium, pH 7.4, at 37 degrees C in an atmosphere of 95% O2/5% CO2. Medium and pituitary TSH was measured by specific RIA (NIDDK-RP-3). Ovariectomy induced a decrease (P < 0.05) in basal TSH release (normal control = 44.1 +/- 7.2; OVX = 14.7 +/- 3.0 ng/ml) and tended to reduce TRH-stimulated TSH release (normal control = 33.0 +/- 8.1; OVX = 16.6 +/- 2.4 ng/ml). The lowest dose of EB (0.7 microgram/100 g body weight) did not reverse this alteration, but markedly increased the pituitary TSH content (0.6 +/- 0.06 microgram/hemipituitary; P < 0.05) above that of OVX (0.4 +/- 0.03 microgram/hemipituitary) and normal rats (0.46 +/- 0.03 microgram/hemipituitary). The intermediate EB dose (1.4 micrograms/100 g body weight) induced a nonsignificant tendency to a higher TSH response to TRH compared to OVX and a lower response compared to normal rats. Conversely, in the rats treated with the highest dose (14 micrograms/100 g body weight), serum 17-beta-estradiol was 17 times higher than normal, and the basal and TRH-stimulated TSH release, as well as the pituitary TSH content, was significantly (P < 0.05) reduced compared to normal rats and tended to be even lower than the values observed for the vehicle-treated OVX group, suggesting an inhibitory effect of hyperestrogenism. In conclusion, while reinforcing the concept of a positive physiological regulatory role of estradiol on the TSH response to TRH and on the pituitary stores of the hormone, the present results suggest an inhibitory effect of high levels of estrogen on these responses.

Paradoxical effect of neuromedin B and thyroxin on thyrotropin secretion from isolated hyperthyroid pituitaries.

Neuromedin B (NB) is a bombesin-like peptide that we recently characterized as a physiological autocrine inhibitor of thyrotropin (TSH) secretion. We now report the effect of NB, thyroxin (T4) and NB + thyroxin on basal and THR (50 nM)-stimulated TSH release from isolated hemipituitaries of hyperthyroid rats. To induce hyperthyroidism, 20 rats were treated with 0.03% methimazole for one month and then received T4, 4 micrograms/100 g body weight, sc, daily for 7 days. Each experimental group consisted of 7 to 9 hemipituitaries. TSH was measured using a rat TSH kit provided by NIDDK. Basal TSH release was paradoxically increased in the presence of 0.1 microM T4 or 0.1 microM NB and even two times higher in the presence of both (Control: 30.0 +/- 4.2 ng/ml; T4: 58.6 +/- 5.6 ng/ml; NB: 53.4 +/- 6.1 ng/ml; T4 + NB: 90.4 +/- 8.5 ng/ml). The percent increment above basal TSH levels after TRH was higher only in the presence of NB (Control: 44.5 +/- 8.2%, NB: 105.3 +/- 18.8%; P < 0.05). Altered responsiveness in hyperthyroidism and direct modification of the intracellular metabolism of T4 are mechanisms that could explain this paradoxical effect.

Paradoxical effect of neuromedin B and thyroxin on thyrotropin secretion from isolated hyperthyroid pituitaries

Neuromedin B (NB) is a bombesin-like peptide that we recently characterized as a physiological autocrine inhibitor of thyrotropin (TSH) secretion. We now report the effect of NB, thyroxin (T4) and NB + thyroxin on basal and THR (50 nM)-stimulated TSH release from isolated hemipituitaries of hyperthyroid rats. To induce hyperthyroidism, 20 rats were treated with 0.03 per cent methimazole for one month and then received T4, 4 micrograms/100 g body weight, sc, daily for 7 days. Each experimental group consisted of 7 to 9 hemipituitaries. TSH was measured using a rat TSH kit provided by NIDDK. Basal TSH release was paradoxically increased in the presence of 0.1 microM T4 or 0.1 microM NB and even two times higher in the presence of both (Control: 30.0 +/- 4.2 ng/ml; T4: 58.6 +/- 5.6 ng/ml; NB: 53.4 +/- 6.1 ng/ml; T4 + NB: 90.4 +/- 8.5 ng/ml). The percent increment above basal TSH levels after TRH was higher only in the presence of NB (Control: 44.5 +/- 8.2 per cent , NB: 105.3 +/- 18.8 per cent ; P < 0.05). Altered responsiveness in hyperthyroidism and direct modification of the intracellular metabolism of T4 are mechanisms that could explain this paradoxical effect