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PubMed2001

Testosterone stimulates growth of tibial epiphyseal growth plate and insulin-like growth factor-1 receptor abundance in hypophysectomized and castrated rats.

Puberty is associated with an increase in the plasma concentration of sex steroids, growth hormone (GH), and insulin-like growth factor-1 (IGF-1). Gonadal steroid hormones are important for the normal pubertal growth spurt and skeletal growth. The mechanism by which gonadal steroids induces skeletal growth is still not fully understood. To study the GH-independent effect of testosterone on growth, we investigated the effect of testosterone injections on the tibial epiphyseal growth plate (EGP) in an in vivo model of hypophysectomized and castrated male rats. Four groups (six animals each) of 28-d-old male rats were studied. Groups A, B, and C were hypophysectomized and castrated and received 500 microg/(kg x d) of hydrocortisone and 15 microg/(kg x d) of levothyroxine sodium. Groups A and B were also treated with daily sc injections of 10 microg of testosterone/100 g of body wt and 100 microg of testosterone/100 g of body wt, respectively, for 7 d. Group C was injected with vehicle alone. Group D were intact animals injected with saline (controls). Animals were sacrificed on 8 d. As expected, serum GH levels were found to be very low (1.13+/-0.1 ng/mL) in the hypophysectomized animals (group C, hypopit), and testosterone treatment did not change them significantly. Serum IGF-1 decreased from 502.9+/-13 ng/mL in group D to 167+/-41.4 ng/mL in group C (p < 0.001). Testosterone therapy had no stimulatory effect on serum IGF-1 levels in the hypopit + low-dose group (A) (220+/-94.8 ng/mL) and had an inhibitory effect in the hypopit + high-dose group (B) (39.3+/-17.5). Histomorphometric determinations demonstrated an EGP width of 472.3+/-39 microm in the intact animals but only 336.9+/-1.6 microm in the hypopit group (C) (p < 0.01). High-dose testosterone treatment (group B) significantly increased the EGP width (to 438.8+/-27.8), (p < 0.001), whereas low-dose testosterone (group A) did not. Immunohistochemistry studies revealed that the levels of IGF-1 in the EGP of the control animals were almost negligible and that testosterone did not change them. However, testosterone increased in a dose-dependent manner the abundance of IGF-1 receptor EGP. We conclude that testosterone has a direct, local, GH-independent effect on the EGP growth and IGF-1 receptor abundance.

Animals↗
PubMed2002

Castration reduces mRNA levels for calcium regulatory proteins in rat heart.

Sex-related differences in the cardiac phenotype have been well established. This study was designed to determine whether androgens regulate myocardial gene expression and play a role in the sex-related differences in the myocardial phenotype. Gonadectomized male rats were treated with testosterone, and myocardial gene expression was examined in whole heart using quantitative real-time PCR. Gonadectomy produced a substantial decrease in mRNA levels for the androgen receptor, Na(+)/Ca(2+) exchanger, L- type calcium channel, and beta(1)-adrenergic receptor (beta(1)AR). Supplementation of testosterone in castrates produced a fivefold increase in androgen receptor mRNA levels. Testosterone treatment of castrates produced almost a sixfold increase in Na(+)/Ca(2+) exchanger mRNA, a tenfold increase in Ltype calcium channel mRNA accumulation, and a fourfold increase in beta(1)AR mRNA levels. Increased calcium channel expression, beta(1)AR expression, and Na(+)/Ca(2+) exchanger expression together may alter cytosolic calcium. These results provide the first evidence that testosterone regulates expression of myocardial calcium regulating genes and thus may play a role in modulating the cardiac phenotype in males.

Animals↗
PubMed2002

Characterization of GH pulsatility in male Shiba goats: effects of postpubertal castration and KP102.

The present study was conducted in order to characterize the secretory pattern of GH in the Shiba goat, a native Japanese miniature goat, and to examine the effects of castration and KP102, a GH secretagogue, on this pattern. Blood samples were taken from an indwelling jugular catheter every 15 min for 24 h, and plasma GH was measured by radioimmunoassay. In intact males, GH was secreted in a pulsatile manner with very regular 5-h periodicity, which consisted of a distinctive GH pulse and a trough of virtually no GH secretion. Postpubertal castration increased the height and decreased the width of GH pulses, though it did not affect the interpulse interval and area under the curve. Modification of the shape of each GH pulse by testicular androgen might play a role in the expression of GH action in the male. KP102 (10 microg/kg, i.v.) immediately induced a robust GH pulse, which was followed by a spontaneous GH pulse of normal characteristics at regular intervals, suggesting that the clock generating GH pulses was reset by KP102. From these observations, we concluded that the Shiba goat is a very suitable experimental model for elucidating the mechanisms underlying GH pulse generation, and in particular, the involvement of androgen and GH secretagogues.

Animals↗
PubMed1988

Sexual differentiation of oxytocin stress responsiveness: effect of neonatal androgenization, castration and a luteinizing hormone-releasing hormone antagonist.

The plasma OT increment following stress in rats is sexually dimorphic, females exhibiting greater responses than males. We have investigated the role of neonatal androgen secretion in determining the sex-typical level of response. Castration of male pups either surgically or functionally (GnRH antagonist treatment) within either 2 h or 5 days of birth did not elevate the OT responses of adult males. In contrast, androgenization of female pups (testosterone, 1.25 mg/pup) within 5 days of birth markedly reduced the OT stress responses of adults to a level insignificantly different to males. The results show that neonatal androgens can exert organizational effects on OT regulatory mechanisms. Since neonatal castration was ineffective it would appear that a prenatal defeminization or masculinization event determines OT stress responsiveness in males.

Animals↗
PubMed1986

Morphine stimulates prolactin release in normal but not in castrated male rats.

Morphine (200 micrograms/rat) was injected intraventricularly (i.v.t.) into normal and into long-term castrated (4 weeks) adult male rats. Animals were killed 10, 20, 40 and 60 min after treatment. In normal animals, the treatment with morphine resulted in a significant increase of serum prolactin concentrations at all time intervals considered. However, the i.v.t. injection of 200 micrograms morphine/rat into castrated rats did not exert any significant effect on prolactin release at any time interval considered. When morphine (200 micrograms/rat) was administered i.v.t. together with the specific opioid receptor blocker naloxone (7.5 or 15 micrograms/rat) the stimulatory effect of morphine on prolactin release was diminished at 10 min, and totally blocked at 20 min. Naloxone given alone did not influence serum prolactin concentrations. The results suggest that the presence of endogenous androgens is essential to permit the stimulatory effect of morphine on prolactin release.

Animals↗
PubMed1987

Gonadotrophin secretion and pituitary responsiveness to LHRH in castrated and intact male rabbits exposed to different photoperiods.

Adult male wild rabbits were exposed to at least 16 weeks of 16L:8 D before experiments began. Plasma LH and FSH concentrations increased significantly (P less than 0.001) when rabbits were castrated in 16L:8D but declined when rabbits were transferred to 8L:16D. Concentrations had returned to normal for castrated rabbits in 16L:8D by 74 days after the start of the 8L:16D treatment. Treatment of intact male rabbits with an injection of LHRH before and after transfer to short daylengths caused a transient increase in plasma LH which lasted 50-80 min and this produced a concomitant rise in plasma testosterone. The daylength change had no effect on this response even though testicular size declined after the transfer to short daylengths. Rabbits moulted in response to exposure to 8L:16D. This suggests that hypothalamic activity responds to photoperiod and that changes in pituitary responsiveness to LHRH and steroid negative feedback are unimportant.

Animals↗
PubMed1992

Effect of testosterone and bovine follicular fluid on concentrations of luteinizing hormone and follicle-stimulating hormone in plasma of castrated rams that are homozygous carriers or non-carriers of the Booroola fecundity gene.

Castrated adult FecBFecB and Fec+Fec+ Booroola rams were injected with charcoal-treated bovine follicular fluid (bFF) (a source of inhibin-like activity) or given testosterone implants to examine whether the fecundity gene (FecB) influences sensitivity to negative feedback hormones in males. Mean concentrations of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) did not differ between genotypes before treatment. In Expt 1, injections of 5 ml bFF, but not of 1 ml (each given four times at intervals of 8 h), significantly (P < 0.05) depressed concentrations of LH and FSH, but there was no effect of genotype. After treatment, gonadotrophin concentrations returned to pretreatment values and for 2-2.5 days scaled (divided by pretreatment mean) LH values (235 +/- 49 for FecBFecB and 96 +/- 26% for Fec+Fec+ rams; P < 0.05) and scaled FSH values (106 +/- 5 for FecBFecB and 85 +/- 5% for Fec+Fec+ rams; P < 0.05) were significantly higher in FecBFecB than in Fec+Fec+ rams in the group that received 5 ml bFF. Irrespective of genotype, treatment with 5 ml bFF did not reduce mean FSH to concentrations observed in testis-intact rams. In Expt 2, Silastic envelopes were implanted subdermally to give physiological or supraphysiological circulating concentrations of testosterone. Both doses significantly reduced scaled LH values in a biphasic manner, such that there was an initial suppression followed by a short-lived increase. During the initial period of suppression in the lower dose group, mean scaled LH values were significantly higher in FecBFecB than in Fec+Fec+ rams (48.3 +/- 7.5 versus 23.1 +/- 5.5%; P < 0.05). Low doses of testosterone decreased LH pulse frequency in both genotypes but decreased (P < 0.05) pulse amplitude and mean concentrations in the Fec+Fec+ animals only. In nonimplanted control rams, mean LH concentrations (in samples taken every 10 min for 12 h) were significantly lower in FecBFecB than in Fec+Fec+ rams (0.6 +/- 0.2 versus 1.3 +/- 0.1 ng ml-1; P < 0.05). The mean FSH response to testosterone was not related to genotype. These data suggest that expression of the FecB gene results in an altered sensitivity of the pituitary gland to changes in negative feedback from testicular hormones and that, irrespective of genotype, neither testosterone nor inhibin-like activity alone can fully control FSH secretion in castrated rams.

Animals↗
PubMed1996

Relaxin in peripheral plasma of boars during development, copulation, after administration of hCG and after castration.

Seventy-two Yorkshire boars were used in five experiments to evaluate the temporal changes in relaxin concentrations in peripheral blood plasma during prepubertal development, copulation, after castration and after treatment with hCG. High concentrations of relaxin (484 +/- 27 pg ml-1) were detected at 11 weeks of age but there was no positive correlation with testicular development. Relaxin concentrations fluctuated in mature boars but the results do not suggest a diurnal rhythm, although there is the possibility of pulsatile secretion. A decrease (P < 0.05) in circulating relaxin was observed before and immediately after copulation. Castration of boars at 90, 115, 160 and 200 days of age did not significantly decrease relaxin concentrations within 48 h. Administration of hCG significantly depressed relaxin secretion at 90 days of age but not at 160 days of age. These studies suggest a non-gonadal source of boar relaxin that is not correlated with testicular growth or testosterone concentrations, is modulated by copulation and by hCG but only at specific stages of development.

Animals↗
PubMed2005

Spontaneous inflammatory pelvic disease in adult non-castrated female rats treated with estrogen.

The adaptive immune response of the genital tract is under the control of sexual steroids; however, the influence of sex hormones on innate immune mechanisms of the genital mucosa are only beginning to be understood. We found that long-term estrogen treatment increases the risk for inflammatory pelvic diseases in adult non-castrated female rats. Female rats (110 g to 130 g) received estrogen (10 rats; 17-beta estradiol, 50 mg pellet; 10 rats: subcutaneous weekly injection of estradiol valerate 0.166 mg/kg). Ten rats received a pellet of 17-beta estradiol and were treated with amoxicillin, 50 mg/kg after the 90th day of exposure to estrogen. Three control groups of ten rats were also used. The estrogen-treated rats developed an inflammatory pelvic disease, with abscess formation after the third month of hormonal treatment. All the surviving animals were killed after six months of hormonal exposure. Among 15 survivors of the two groups that received estrogen 13 animals presented tuboovarian abscesses. Among eight survivors of the group treated with amoxicillin, six had tuboovarian abscesses. None of the 30 control rats presented macro or microscopic signs of inflammatory disease in the uterus, tubes or ovaries. We conclude that estrogen impairs the defense mechanisms of the genital tract of non-castrated female rats, enhancing bacterial growth in the vagina and ascending infection to the uterus, tubes and ovaries.

Amoxicillin↗
PubMedDate not supplied

Comparative therapeutic use of Risedronate and Calcarea phosphorica--allopathy versus homeopathy--in bone repair in castrated rats.

Osteoporosis, a disease characterized by progressive bone loss, has been the target of several studies in the past few years. It results in a much higher risk for fractures and might cause slower bone lesion healing. The aim of this work was to study the effects of Risedronate (allopathic medicine) and Calcarea phosphorica 6CH (homeopathic medicine) on the repair of bone lesions in male rats with osteoporosis induced by castration. Eighty-four three-month-old rats were used divided into four groups of twenty-one animals each. Three groups where castrated and one group was submitted to Sham surgery. One month later, cortical lesions were made in all animals' tibiae and, after one day, the different experimental treatments began according to the following groups: CR--castrated/Risedronate (1 mg/kg/day); CCp--castrated/Calcarea phosphorica 6CH (3 drops/day); CP--castrated/placebo and SP--Sham/placebo. The animals were sacrificed at seven, fourteen and twenty-eight days after the beginning of the treatments and had their tibiae removed. Digital radiographs of the tibiae were taken and analyzed in order to evaluate the optical density of the defect area. Then, they were decalcified and processed for histological and histomorphometrical analysis. The data were submitted to ANOVA, and to the Tukey and Dunnett tests (5%). The allopathic and homeopathic treatments led to different bone formation as regards remodeling and maturation aspects. Further research is necessary to access the resistance and quality of the newly formed bone.

Analysis of Variance↗
PubMed1985

Effects of photoperiod, pinealectomy and castration on body weight and daily torpor in Djungarian hamsters (Phodopus sungorus).

During the autumn and winter Djungarian hamsters (Phodopus sungorus) exhibit regression of the gonads, development of a white winter pelage, loss of body weight and daily torpor. These seasonal events are largely regulated by changes in photoperiod. The present experiments were designed to examine the role of the testes and the pineal gland in photoperiodically induced daily torpor and body weight loss. Hamsters displayed a loss of body weight and daily torpor when exposed to a short-day photoperiod in a cold environment, but these phenomena did not occur in hamsters exposed to long days and cold. Testicular regression is probably a precondition for the display of torpor, since daily torpor was almost totally inhibited in hamsters which were exposed to short days and in which testosterone was administered from subcutaneous silicone elastomer implants. Nevertheless, decreased testosterone secretion alone is not a sufficient condition for induction of daily torpor, since torpor was rarely observed in hamsters exposed to long days, even after castration. In addition to decreased testicular activity, the pineal gland is also involved in establishing conditions for torpor. Thus, pinealectomy prevented the display of torpor by castrated hamsters exposed to short days. Body weight changes were also found to be influenced by both testicular hormone and pineal activity. These observations indicate that the pineal gland is involved, as a part of the photoperiodic mechanism, in regulating a variety of physiological events and that some of these actions of the pineal are independent of its extensively described actions on the reproductive axis.

Adaptation, Physiological↗
PubMed1986

Minimal effects of 17 beta-hydroxy-17 alpha-methyl-estra-4,9,11-triene-3-one (R1881) on sexual behaviour in prepubertally castrated rams.

Ten adult prepubertally castrated rams were injected with 5 alpha-dihydrotestosterone propionate (DHTP; 20 mg/day) for 3 weeks to stimulate genital development. Thereafter, half of the sheep were injected with testosterone (100 mg/day) for a further 4 weeks, while the remainder received the same dose of 17 beta-hydroxy-17 alpha-methyl-estra-4,9,11-triene-3-one (methyltrienolone; R1881). All the animals were tested for sexual behaviour on 15 occasions with ovariectomized ewes in which oestrous behaviour was induced by injections of 50 micrograms oestradiol-17 beta benzoate at 4- to 5-day intervals. Behavioural tests were of 10 min duration and were carried out thrice weekly over a 5-week period, starting in the final week of DHTP treatment. Animals treated with testosterone showed a highly significant increase in courtship behaviour (tongue-flicks; lunges and nudges) after only four daily injections and this level of activity was maintained to the end of the experiment. However, the incidence of courtship activity in sheep treated with R1881 was similar to that recorded during the period of DHTP treatment. All animals given testosterone displayed mounts with pelvic thrusts and erections, and achieved intromission with ejaculation. These activities remained significantly more frequent than in sheep treated with R1881, starting from tests 9, 8 and 12 respectively. Four of the five individuals in the group given R1881 showed occasional mounts with thrusts, three showed sporadic erections and one sheep intromitted in the final test. These results indicate that, in contrast to the rat, R1881 has only very weak effects on sexual behaviour in the castrated ram.

Animals↗
PubMed1986

Activation of sexual behaviour in castrated rats: the role of oestradiol.

Sexual behaviour was induced in castrated male rats with oestradiol-17 beta- or testosterone-filled constant-release implants. Testosterone-induced sexual behaviour was unaffected by treatment with the 5 alpha-reductase inhibitor 17 beta-N,N-diethylcarbamoyl-4-aza-5 alpha-androstan-3-one (4-MA; 16.7 mg/day) but treatment with the aromatization inhibitor 1,4,6-androstatriene-3,17-dione (ATD; 10 mg/day) prevented testosterone from inducing the behaviour. Sexual behaviour could be activated in castrated rats treated with testosterone plus ATD by treatment with 4-MA or with implants filled with a low dose of oestradiol. Lordosis behaviour induced in ovariectomized rats with testosterone-filled implants and progesterone was blocked by ATD treatment and could not be activated with 4-MA but oestradiol implants restored the display of lordosis in the testosterone plus ATD-treated females. 4-MA inhibited the in-vitro formation of [14C]5 alpha-dihydrotestosterone from [14C]testosterone by combined preoptic and hypothalamic tissue at all doses tested and a high dose of oestradiol exerted a similar effect. The results suggest that androgen aromatization is required for testosterone-activated female sexual behaviour but not for testosterone-activated male sexual behaviour. It is suggested that oestradiol normally acts to control the sexual behaviour of male rats by modifying neural androgen metabolism.

Androgens↗
PubMed1987

The role of the hypothalamic beta-adrenergic system in controlling the LH rise in short-term castrated rats.

Intraventricular infusions of adrenaline and various pharmacological agents acting on beta-adrenergic receptor subtypes were carried out in rats orchidectomized 16 h previously. Infusions (10 microliter) of solutions containing the drugs were administered under anaesthesia induced with alphaxalone and alphadolone. Levels of LH were measured in plasma collected immediately before and at predetermined intervals after the infusion. The acute rise in LH levels after castration was increased still further by isoprenaline (a mixed beta 1- and beta 2-agonist), fenoterol (a beta 2-agonist) and atenolol (a beta 1-antagonist). In contrast, prenalterol (a beta 1-agonist) and (2RS,3RS)-3-isopropylamino-1-(7-methylindan-4-yloxy)++ +butan-2-ol (ICI 118,551) (a selective beta 2-antagonist) were inhibitory to LH release. Adrenaline itself, salbutamol (another selective beta 2-agonist), propranolol (a mixed beta-antagonist) and metoprolol (a beta 1-antagonist) did not significantly alter plasma LH concentrations at the doses administered. The stimulatory effect of isoprenaline on LH release was partially reduced when given together with ICI 118,551, but was not affected when administered simultaneously with atenolol. The inhibitory effect of ICI 118,551 was, however, prevented by concomitant administration with fenoterol, as was that of prenalterol when infused with atenolol. The results suggest that the hypothalamic mediation of the short-term changes in LH release in response to castration is exerted, at least in part, through the activation of a beta 2-stimulatory component and the suppression of a beta 1-inhibitory component.

Adrenergic beta-Agonists↗
PubMed1987

Anaesthesia with alphaxalone plus alphadolone acetate decreases serum concentrations of LH in castrated rats.

Alphaxalone is considered the anaesthetic of choice in neuroendocrine reproductive studies in female rats, since it appears to have little, if any, effect on release of gonadotrophin-releasing hormone. There has been less study of the effects of this anaesthetic on the male reproductive neuroendocrine axis, however. Accordingly, the time-dependent effects of alphaxalone, as well as of urethane and ketamine, on the increased levels of LH in castrated rats were determined. Each anaesthetic was administered i.p. and each depressed LH levels significantly compared with those in castrated unanaesthetized rats killed by decapitation (controls). The effect of the anaesthetics was noted 15 min after administration and persisted at 30 and 60 min in animals anaesthetized with alphaxalone and urethane. Only in ketamine-anaesthetized animals did serum concentrations of LH finally rise to concentrations not significantly different from those in control rats. Thus alphaxalone, though useful in female neuroendocrine studies, is as profoundly disruptive as other anaesthetics on the male rat hypothalamic-pituitary reproductive unit.

Anesthetics↗
PubMed1988

Effects of progestins on sexual behaviour in castrated lizards (Cnemidophorus inornatus).

In many male vertebrates, androgens stimulate, while progesterone inhibits, sexual behaviour. Testicular androgens also control sexual behaviour in males of the lizard Cnemidophorus inornatus. However, administration of progesterone will reinstate sexual behaviour in castrated animals. Increased doses of progesterone did not result in increased numbers of responders; at all doses tested approximately 36% (n = 45) of animals treated with progesterone responded as reliable courters. A high percentage (60-68%) of progesterone-sensitive individuals maintained their sensitivity over a period of months. A synthetic progestin 17,21-dimethyl-19-nor-4,9-pregnadiene-3,20-dione with low rates of metabolism and conversion, also stimulated sexual behaviour in castrated C. inornatus. Finally, the synthetic antiprogestin 11 beta-4-dimethylaminophenyl-17 beta-hydroxy-17 alpha-1-propinyl- 4,9-oestradiene-3-one inhibited the stimulatory effects of progesterone on sexual behaviour but failed to inhibit the stimulatory effects of androgens. These findings indicate an unusual departure from the characteristic pattern of steroid sensitivities of neural centres controlling sexual behaviour.

Animals↗
PubMed1988

Oestradiol synergizes with 5 alpha-dihydrotestosterone or 3 alpha- but not 3 beta-androstanediol in inducing sexual behaviour in castrated rats.

Castrated male rats were treated with constant-release implants filled with testosterone, oestradiol-17 beta, 17 beta-hydroxy-5 alpha-androstan-3-one (5 alpha-dihydrotestosterone; DHT), 5 alpha-androstane-3 alpha, 17 beta-diol (3 alpha-Adiol) or 5 alpha-androstane-3 beta,17 beta-diol (3 beta-Adiol). Only testosterone activated the sexual behaviour of the rats. If combined with oestradiol, DHT or 3 alpha-Adiol induced the behaviour, but 3 beta-Adiol failed to have this effect. Oestradiol inhibited the in-vitro formation of [14C]Adiols from [14C]DHT by combined preoptic and hypothalamic tissue, but only when given in high doses. No effect on the formation of [14C]Adiols from [14C]DHT was found in rats treated in vivo with DHT or with the combination of DHT and oestradiol which effectively stimulated sexual behaviour. These results do not support the suggestion that oestradiol may synergize with androgens to induce sexual behaviour in castrated rats by inhibiting androgen metabolism.

Androstane-3,17-diol↗
PubMed1993

Human recombinant inhibin A and testosterone act directly at the pituitary to suppress plasma concentrations of FSH in castrated rams.

The roles of inhibin and testosterone in the negative feedback control of the secretion of FSH were explored in experiments using castrated rams administered human recombinant inhibin A (hr-inhibin) and testosterone propionate (TP). Two experiments were conducted in the non-breeding season. In experiment 1, two groups of long-term castrated rams (wethers) were treated with an i.v. injection of either vehicle or hr-inhibin in two doses (25 and 50 micrograms) given 2 weeks apart. Plasma concentrations of FSH, measured by radioimmunoassay, were suppressed significantly (P < 0.01) and equally by both doses of hr-inhibin with a mean (+/- S.E.M.) maximal suppression of FSH of 19.9 +/- 2.60% occurring 6-10 h after injection. In experiment 2, hypothalamo-pituitary disconnected (HPD) wethers given 125 ng gonadotrophin-releasing hormone (GnRH) every 2 h, were treated with vehicle or 25 or 50 micrograms hr-inhibin before or after treatment (32 mg/day) with TP. A cross-over design was used so that each wether was treated with vehicle and hr-inhibin. Treatment with TP significantly (P < 0.001) suppressed plasma concentrations of FSH by 56%. Both doses of hr-inhibin were similarly effective in significantly (P < 0.05) suppressing plasma concentrations of FSH causing a mean suppression of 31.1 +/- 5.60% 6-10 h after injection. The suppressive effect of hr-inhibin was significantly (P < 0.05) increased when the wethers were treated with TP to a mean suppression of 50.7 +/- 5.6% 6-10 h after injection.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗