Elevated testosterone level in response to clomiphene in male Anolis carolinensis

Anolis carolinensis were used as experimental models to study the short-term effects of the fertility drug, clomiphene citrate, on male squamate reproductive function. Daily injections of 10.0 micrograms of clomiphene induced an increase in plasma testosterone over a 5 day period. No change in testis mass or morphology was elicited over this time.     

Use of clomiphene and luteinizing hormone/follicle stimulating hormone-releasing hormone in investigation of ovulatory failure.

A luteinizing hormone/follicle-stimulating hormone-releasing hormone (LH/FSH-RH) test was performed in 70 women with amenorrhoea or anovulatory infertility, or both, and a clomiphene stimulation test was also performed in 24 of these patients. Most patients responded to LH/FSH-RH with significant increases in LH and FSH. In women with gonadal dysgenesis or premature ovarian failure exaggerated responses were observed after LH/FSH-RH and there was no change in high basal LH levels after clomiphene. Patients with absent or impaired responses to LH/FSH-RH failed to respond to clomiphene. All patients with anovulatory menstrual cycles responded to both LH/FSH-RH and clomiphene, while seven out of 13 amenorrhoeic patients with a normal LH/FSH-RH response showed an early LH rise during clomiphene treatment and six were unresponsive. These results suggest a difference between the two groups at hypothalamic level with consequent therapeutic implications.     

Changes of hormonal function of the adrenal and gonadal glands in baboons of different age groups

The purpose of this study was to characterize the changes of hormonal function of the adrenals and gonads during aging in male baboons ( Papio hamadryas ). Basal levels of plasma dehydroepiandrosterone, dehydroepiandrosterone sulfate, pregnenolone, and 17-hydroxypregnenolone progressively decrease with age from 10–15 years when analyzed by specific radioimmunoassay. However, no significant changes were found in cortisol and 11-desoxycortisol concentrations. The levels of sexual hormones did not differ in young and mature groups. In the 20–26-year-old animals, the concentration of testicular androgens showed a tendency to decrease, while the concentration of biologically active luteinizing hormone (LH) showed a tendency to increase. The old animals exhibited a decrease of plasticity of the pituitary–testicular system, which was manifested in the deceleration of the decrease of LH and T concentrations after the peak values had been reached in response to luteinizing hormone-releasing hormone (LHRH) administration. The oldest male also developed some refractoriness of the pituitary–gonadal system to the prolonged administration of LHRH agonist. The hormonal imbalance which develops with age may play an important role in the age-related involutional process.     

Pituitary response to exogenous LHRH in superovulated women

The response of the pituitary to exogenous LHRH was investigated in 9 normally ovulating women during the late follicular phase of a spontaneous (control) cycle, a cycle during treatment with clomiphene and a cycle during treatment with 'pure' FSH. During clomiphene treatment, basal FSH concentrations increased significantly up to Day 6 of the cycle and then decreased progressively while basal LH values showed a continuous rise. During treatment with FSH, basal LH concentrations decreased significantly. The response of both FSH and LH to LHRH showed a significant and quantitatively similar decrease during clomiphene or FSH administration as compared to the spontaneous cycles. It is suggested that basal secretion of FSH and LH is regulated by two separate mechanisms, and that an ovarian inhibitory factor(s) attenuates the response of both FSH and LH to exogenous LHRH and possibly the endogenous LH surge in superovulated cycles.     

Estrogenic and antiestrogenic properties of clomiphene citrate in laboratory mice

The estrogen agonistic and antagonistic properties of clomiphene citrate were investigated in the mice. Clomiphene citrate was tested at various doses of 0.1, 1.0, 10 and 100 μg for three consecutive days in immature and mature bilaterally ovariectomized mice. Clomiphene citrate showed uterotrophic activity in both immature and ovariectomized conditions. The lower doses of 0.1 and 1.0 μg were ineffective to show any uterotrophic stimulation. Clomiphene citrate at 10 μg dose produced 305.56% increase in uterine weight i.e., 27.70 ± 0.24 vs 6.83 ± 0.06 in immature and 182.27% i.e., 42.68 ± 1.12 vs 15.12 ± 0.57 in ovariectomized mice. Clomiphene citrate at 100 μg dose showed significant uterotrophic effect e.g., 435.57% i.e., 36.58 ±0.34 vs 6.83 ± 0.06 in immature and 586% i.e., 103.80 ± 0.60 in ovariectomized mice. When clomiphene citrate was administered in combination with 0.32 μg of estradiol 17-β it caused significant antagonistic effect (decrease in uterine weight) at 10 and 100 μg respectively. Clomiphene citrate at 10 μg dose produced 32% i.e., 28.93 ± 0.43 vs 38.04 ± 2.68 in immature and 35% i.e., 59.64±1.44 vs 83.34 ±0.25 in ovariectomized mice respectively. Histological observation clearly showed that clomiphene citrate at 10 and 100 μg doses did not cause any differential hypertrophy of the epithelial layer. Similar doses in combination with estradiol produced significant antagonistic effect on uterine weight and luminal epithelial cell height.     

Clomiphene, an ovulation-inducing agent, mobilizes intracellular Ca2+ and causes extracellular Ca2+ influx in bladder female transitional carcinoma cells

BACKGROUND/METHODS: The effect of clomiphene, an ovulation-inducing agent, on cytosolic free Ca2+ levels ([Ca2+]i) in populations of BFTC human bladder cancer cells was explored by using fura-2 as a Ca2+ indicator. RESULTS: Clomiphene at concentrations between 10 and 75 microM increased [Ca2+]i in a concentration-dependent manner and the signal saturated at 50 microM. The [Ca2+]i signal was biphasic with an initial rise and a slow decay. Ca2+ removal inhibited the Ca2+ signal by about 40-50% in maximum [Ca2+]i. Adding 3 mM Ca2+ increased [Ca2+]i in cells pretreated with 50 microM clomiphene in Ca2+-free medium, suggesting that clomiphene induced capacitative Ca2+ entry. In Ca2+-free medium, pretreatment with 50 microM brefeldin A (to disrupt the Golgi complex Ca2+ store), 1 microM thapsigargin (to inhibit the endoplasmic reticulum Ca2+ pump), and CCCP (to uncouple mitochondria) inhibited 85% of clomiphene-induced intracellular Ca2+ release. Conversely, pretreatment with 50 microM clomiphene in Ca2+-free medium abolished the [Ca2+]i increase induced by brefeldin, thapsigargin or CCCP. The intracellular Ca2+ release was unaltered by inhibiting formation of inositol-1,4,5-trisphosphate (IP3) with 2 mM 1-(6-((17beta-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione (U73122; a phospholipase C inhibitor). CONCLUSION: The [Ca2+]i increase induced by 50 microM clomiphene was not affected by 10 microM of nifedipine, verapamil or diltiazem. Collectively, the results suggest that clomiphene releases intracellular Ca2+ in an IP3-independent manner and also activates extracellular Ca2+ influx.     

Effect of clomiphene on Ca(2+) movement in human prostate cancer cells

The effect of clomiphene, an ovulation-inducing agent, on cytosolic free Ca(2+) levels ([Ca(2+)](i)) in populations of PC3 human prostate cancer cells was explored by using fura-2 as a Ca(2+) indicator. Clomiphene at concentrations between 10-50 microM increased [Ca(2+)](i) in a concentration-dependent manner. The [Ca(2+)](i) signal was biphasic with an initial rise and a slow decay. Ca(2+) removal inhibited the Ca(2+) signal by 41%. Adding 3 mM Ca(2+) increased [Ca(2+)](i) in cells pretreated with clomiphene in Ca(2+)-free medium, confirming that clomiphene induced Ca(2+) entry. In Ca(2+)-free medium, pretreatment with 50 microM brefeldin A (to permeabilize the Golgi complex), 1 microM thapsigargin (to inhibit the endoplasmic reticulum Ca(2+) pump), and 2 microM carbonylcyanide m-chlorophenylhydrazone (to uncouple mitochondria) inhibited 25% of 50 microM clomiphene-induced store Ca(2+) release. Conversely, pretreatment with 50 microM clomiphene in Ca(2+)-free medium abolished the [Ca(2+)](i) increase induced by brefeldin A, thapsigargin or carbonylcyanide m-chlorophenylhydrazone. The 50 microM clomiphene-induced Ca(2+)release was unaltered by inhibiting phospholipase C with 2 microM 1-(6-((17beta-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione (U73122). Trypan blue exclusion assay suggested that incubation with clomiphene (50 microM) for 2-15 min induced time-dependent decrease in cell viability by 10-50%. Collectively, the results suggest that clomiphene induced [Ca(2+)](i) increases in PC3 cells by releasing store Ca(2+) from multiple stores in an phospholipase C-independent manner, and by activating Ca(2+) influx; and clomiphene was of mild cytotoxicity.     

The relationship between sleep circadian rhythm and central feedback mechanism of gonadal steroid in female guinea pigs

To examine the relationship between the sleep rhythm and the gonadal feedback system in the guinea pig, the effects of estrous cycle, gonadal steroids and brain deafferentiations on the sleep rhythm were studied and the following results were obtained; 1) the guinea pigs did not show an apparent circadian rhythmicity in the sleep-wakefulness cycle but showed an ultradian rhythm, whereas, the activity rhythm was circadian, 2) the rhythm in paradoxical sleep(PS) showed changes associated with the estrous cycle which were characterized by a decrease and rebound-like increase in PS amounts on the day of proestrus, 3) the horizontal deafferentation above the medial preoptic area at the level of the anterior commissure (MPO roof cut) did not disrupt the estrous cycle dependent changes in the PS rhythm, but the prechiasmatic deafferentiation of the medial basal hypothalamus (PCD) and the large complete deafferentation of the medial basal hypothalamus (CDL) disrupted them, 4) ovariectomy (OVX) did not result in any changes in sleep and activity rhythms, 5) an administration of estradiol benzoate (E2) to OVX guinea pig caused a decrease in the amount of PS and an administration of progesterone (P) 48h after E2 caused a more pronounced decrease and rebound-like increase in the amount of PS, 6) the MPO roof cut did not affect the steroidal modification of the PS rhythm and the PCD disrupted it, while the CDL-animal also showed a E2-induced PS decrease. From these results, it appears that the guinea pig may be a circadian animal, but this may not be seen in the sleep-wakefulness cycle, and the estrous cycle dependent changes in the PS rhythm may be the reflection of steroidal modification of the sleep rhythm and the site of action may be the inside of the medial preoptic anterior hypothalamic structures, but this area may also be affected by the output from the medial basal hypothalamus.     

Induction of hyaluronic acid synthetase by estrogen in the mouse skin

Hyaluronic acid synthetase activity was measured in male mouse skin following the topical application of estradiol in vivo. The enzyme activity increased in parallel with the hyaluronic acid content of the skin, and showed a similar response in the skin of ovariectomized female mice. The increase in enzyme activity was reduced by the anti-estrogen agents, tamoxifene citrate and clomiphene citrate, which block competitively the binding of estrogen to the estrogen receptor. The increase in hyaluronic acid synthetase activity was also reduced by topical application of cycloheximide or by subcutaneous injection of actinomycin D. The results suggest that the stimulation of hyaluronic acid synthesis in mouse skin in response to estrogen treatment is mediated through estrogen receptors and involves the induction of the enzyme hyaluronic acid synthetase.     

Changes induced in adrenergic lipolysis by the administration of diethylstilboestrol, oestradiol and clomiphene

The authors studied changes in adrenergic lipolysis in the epididymal adipose tissue of rats to which diethylstilboestrol and oestradiol combined with the anti-oestrogen clomiphene were administered. The maximum lipid-mobilizing effect of isoprenaline was increased not only by subcutaneously administered diethylstilboestrol, but also by the highest dose of the antioestrogen clomiphene used (p.o., 200 micrograms.kg-1 b.w.). Under the given experimental conditions, with 4 1/2 h incubation of adipose tissue, clomiphene was also effective when added in vitro. Its own oestrogenic effect probably stimulated the lipid-mobilizing action of isoprenaline. On combining the administration of increasing doses of clomiphene (p.o., 1-5 days) with a constant dose of oestradiol (200 micrograms.kg-1, s.c. on the 8th day, i.e. 24 h before the actual experiment), changes in isoprenaline lipolysis depended on the dose of clomiphene. In low doses clomiphene inhibited the stimulating effect of subsequently administered oestradiol on isoprenaline-induced lipolysis, but in large doses (100 and 200 micrograms.kg-1 daily) it potentiated, together with oestradiol, the lipid-mobilizing effect of isoprenaline. The results show that the non-steroid oestrogen diethylstilboestrol and the antioestrogen clomiphene may be included among the hormones capable of altering the response of adipose tissue to sympathomimetics (isoprenaline). We attribute the fact that clomiphene acted either as an antagonist or as an agonist of oestradiol to its combined oestrogenic and anti-oestrogenic effects.     

Inhibition of decidual induction in rats by clomiphene and tamoxifen.

The objective of this study was to characterize the estrogen action that confers endometrial sensitization to nontraumatic deciduogenic stimuli by use of antiestrogens. Tamoxifen, ethamoxytriphetol, and clomiphene and its two component enantiomers inhibited decidual induction in pseudopregnant rats when administered 17 h before pyrathiazine. Unexpectedly, clomiphene (250 micrograms/rat) and tamoxifen (25 micrograms/rat) proved inhibitory at all times up to and including the time of induction. Clomiphene, administered in the hours preceding decidual induction, inhibited the increase of ornithine decarboxylase activity, which normally marks the end of the induction phase. Clomiphene had no inhibitory effect on the availability or receptor binding of progesterone. Clomiphene also inhibited implantation of blastocysts when administered at the time of their adherence to the uterus. The inhibition by antiestrogens of decidual induction could not be explained on the basis of the current understanding of mechanisms of estrogen action. The discrepancies were that no latent period between the time of antiestrogen administration and decidual induction was observed and no difference was observed in the inhibitory activities of the isomers of clomiphene.     

Effect of clomiphene on Ca movement in human prostate cancer cells

The effect of clomiphene, an ovulation-inducing agent, on cytosolic free Ca²⁺ levels ([Ca²⁺]_i) in populations of PC3 human prostate cancer cells was explored by using fura-2 as a Ca²⁺ indicator. Clomiphene at concentrations between 10-50 μM increased [Ca²⁺]_i in a concentration-dependent manner. The [Ca²⁺]_i signal was biphasic with an initial rise and a slow decay. Ca²⁺ removal inhibited the Ca²⁺ signal by 41%. Adding 3 mM Ca²⁺ increased [Ca²⁺]_i in cells pretreated with clomiphene in Ca²⁺-free medium, confirming that clomiphene induced Ca²⁺ entry. In Ca²⁺-free medium, pretreatment with 50 μM brefeldin A (to permeabilize the Golgi complex), 1 μM thapsigargin (to inhibit the endoplasmic reticulum Ca²⁺ pump), and 2 μM carbonylcyanide m-chlorophenylhydrazone (to uncouple mitochondria) inhibited 25% of 50 μM clomiphene-induced store Ca²⁺ release. Conversely, pretreatment with 50 μM clomiphene in Ca²⁺-free medium abolished the [Ca²⁺]_i increase induced by brefeldin A, thapsigargin or carbonylcyanide m-chlorophenylhydrazone. The 50 μM clomiphene-induced Ca²⁺release was unaltered by inhibiting phospholipase C with 2 μM 1-(6-((17β-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione (U73122). Trypan blue exclusion assay suggested that incubation with clomiphene (50 μM) for 2-15 min induced time-dependent decrease in cell viability by 10-50%. Collectively, the results suggest that clomiphene induced [Ca²⁺]_i increases in PC3 cells by releasing store Ca²⁺ from multiple stores in an phospholipase C-independent manner, and by activating Ca²⁺ influx; and clomiphene was of mild cytotoxicity.     

Medium from irradiated cells induces dose-dependent mitochondrial changes and BCL2 responses in unirradiated human keratinocytes

Exposure of unirradiated human keratinocytes to irradiated cell conditioned medium (ICCM) is known to cause a cascade of events that leads to reproductive death and apoptosis. This study investigates the effect of ICCM on clonogenic survival, mitochondrial mass and BCL2 expression in unirradiated keratinocytes. Exposure to 5 mGy, 0.5 Gy and 5 Gy ICCM resulted in a significant decrease in clonogenic survival. Human keratinocytes incubated with ICCM containing an antioxidant, N-acetylcysteine, showed no significant decrease in clonogenic survival. HPV-G cells incubated with ICCM containing a caspase 9 inhibitor showed no significant decrease in clonogenic survival when the ICCM dose was < or =0.5 Gy. A significant increase in mitochondrial mass per cell was observed after exposure to 5 mGy and 0.5 Gy ICCM. A change in the distribution of the mitochondria from a diffuse cytoplasmic distribution to a more densely concentrated perinuclear distribution was also observed at these doses. No significant increase in mitochondrial mass or change in distribution of the mitochondria was found for 5 Gy ICCM. Low BCL2 expression was observed in HPV-G cells exposed to 5 mGy or 0.5 Gy ICCM, whereas a large significant increase in BCL2 expression was observed in cells exposed to 5 Gy ICCM. This study has shown that low-dose irradiation can cause cells to produce medium-borne signals that can cause mitochondrial changes and the induction of BCL2 expression in unirradiated HPV-G cells. The dose dependence of the mitochondrial changes and BCL2 expression suggests that the mechanisms may be aimed at control of response to radiation at the population level through signaling pathways.     

DNA breakage of human leukemia cells by clomiphene, an ovulation-inducing agent

When HPB-ALL, human lymphoblastic leukemia cells were treated with clomiphene citrate, an ovulation-inducing agent, poly(ADP-ribose) synthesizing activity of the cells increased up to 4 fold. This stimulatory effect was almost comparable to that of bleomycin, a typical DNA strand breaking agent. Since the agents causing DNA breakage stimulate poly(ADP-ribose) synthesis in cells [Berger, N. A., Sikorski, G. W., Petzold, S. J., and Kurohara, K. K. J. Clin. Invest. 63, 1164-1171 (1979)], clomiphene citrate is suggested to damage DNA of the cells. In fact, an increase of single strand breakage of the DNA was detected by using alkaline sucrose density gradient centrifugation when the HPB-ALL cells were treated with increasing concentration of clomiphene. The inhibition of the cell growth by clomiphene citrate (IC50 = 5 micrograms/ml) appeared to be ascribable to its potent DNA-damaging effect. Although bleomycin activated purified poly(ADP-ribose) synthetase by cleaving covalently closed circular plasmid pBR322 DNA in vitro, clomiphene citrate per se did not.     

Inhibition of androgen and oestrogen production by clomiphene citrate in avian theca cells

Isolated theca cells (2 X 10(5)/ml) were pre-incubated for 1 h in the presence or absence of clomiphene citrate (10(-12)-10(-4) M). Ovine LH (50 ng/ml) was added and cells were incubated for an additional 3 h. A 50% inhibition of LH-stimulated androstenedione and oestrogen production was obtained with doses of 10(-8) M and 2 X 10(-7) M clomiphene, respectively. Furthermore, the effect of clomiphene on LH-stimulated androstenedione production was reversed by washing clomiphene from the cells before stimulation with LH. In subsequent experiments, the effects of clomiphene on C17-20-lyase and aromatase activities were examined. Conversion of [3H]17-hydroxyprogesterone to androstenedione was inhibited by 50% when theca cells were pretreated with 10(-5) M-clomiphene. In addition, conversion of testosterone to oestrogen by theca cells was inhibited in a dose-dependent manner by clomiphene, with 50% inhibition occurring at a dose of 5 X 10(-6) M. The results show that clomiphene treatment in vitro inhibits androgen and oestrogen production in theca cells by inhibitory effects on the activities of C17-20-lyase and aromatase. In addition to the widely-accepted effects of clomiphene on the hypothalamic-pituitary axis, the present findings add further support to the suggestion that clomiphene exerts direct effects on ovarian steroidogenesis.     

Cytokinins in cut carnation flower III. The influence of indoleacetic acid on growth,cytokinin content and metabolism of 14C-benzyladenine in cultured ovaries

Exogenous applications of auxin to in vitro grown carnation ovaries resulted in an increase in dry mass and a decrease in the levels of endogenous cytokinins within the ovaries. Untreated ovaries showed no significant increase in dry mass. There was however, an increase in endogenous cytokinins over the same period. When ¹⁴C-BA was applied to ovaries both with and without exogenous auxin the pattern of growth and cytokinin changes followed a similar trend. Although the BA-metabolites were similar in both treatments, degradative metabolism of the cytokinin was faster and the increase in ovary dry mass greater when auxin was included in the treatment.     

长期强迫运动对大绒鼠体重、能量代谢和血清瘦素的影响

动物稳定体重的维持需要能量摄入和消耗之间的平衡。运动是影响动物能量平衡的重要因素之一。为了解运动对大绒鼠(Eothenomys miletus)的生理学效应,在室内条件下,测定了强迫运动训练(运用小鼠封闭跑台)8周后大绒鼠的体重、代谢率、摄入能、血清瘦素和身体组成的变化。结果显示,强迫运动训练8周对大绒鼠的体重无显著影响;大绒鼠的代谢率和摄入能均显著增加,训练8周后静止代谢率较对照组增加了29.9%,运动最大代谢率较对照组增加了10.7%;强迫运动训练8周组的身体脂肪重量比对照组降低了28.9%,血清瘦素水平比对照组下降了27.4%,对照组的瘦素与体脂含量具有明显的相关性,但运动组则不具有相关性;运动组的肝重量和消化道重量较对照组均显著增加;而体水重量则显著降低。这些结果表明,在强迫运动训练期间大绒鼠主要通过动员储存的脂肪、增加代谢率和食物摄入的方式来维持自身的体重及能量平衡。瘦素在长期强迫运动过程中对身体脂肪含量的变化具有调节作用。     

Protein- and tryptophan-restricted diets induce changes in rat gonadal hormone levels

The release of gonadotrophic hormones starts at puberty and, along with the subsequent estral cyclicity, is subject to hormonal feedback systems and to the action of diverse neuroactive substances such as gamma amino butyric acid and catecholamines. This study shows the effect of the administration during 40 days of protein-restricted and corn-based (tryptophan- and lysine-deficient) diets on the serotonin concentration in medial hypothalamic fragments as well as in follicle-stimulating luteinizing hormones, 17-beta-estradiol and progesterone serum levels, and estral cyclicity in 60- and 100-day-old rats (young, mature, and in gestation). In young rats, a delay in vaginal aperture development, and a lengthening of the estral cycle to a continuous anestral state was observed, mainly in the group fed corn. This group showed a 25% decrease in the serotonin concentration compared with the protein-restricted group, which exhibited an increase of 9% over the control group. Luteinizing hormone levels decreased in 16% and 13%, whereas follicle-stimulating hormone increased in 13% and 5% in the young animals of restricted groups, respectively, compared with the control group. Serum progesterone levels decreased only in young restricted versus control animals, and no differences were seen among adult and gestational rats. Serum levels of 17-beta-estradiol in restricted animals showed different concentration patterns, mainly in the corn group, which was higher at the 20th gestational day, falling drastically postpartum. The results obtained in this study show serotonin to be a very important factor in the release of gonadotrophic hormones and the start of puberty.     

The effect of calcitonin on prolactin secretion during gestation

The relationship between calcitonin (CT) and prolactin (PRL) was studied by means of the injection of salmon calcitonin (SCT) i.p. on day 1 of gestation. An estrogen inhibitor - clomiphene - was also administered to certain groups of animals on day 4 and 5 of gestation. SCT did not affect PRL levels on day 1 of gestation nor on days 5 or 7, but it prevented the rise of PRL levels observed in animals submitted to injection stress on days 4 and 5. In animals treated with clomiphene, the inhibition by SCT on PRL increase after injection stress was partially abolished. SCT while not affecting basal PRL level prevented the rise observed after stress and this effect occurred some days later. Thus SCT could exercise a delayed neuroendocrine control. This action of SCT seemed to be partially dependent upon the presence of estrogens.     

Flight-oogenesis syndrome in a blood-sucking bug: biochemical aspects of lipid metabolism

Lipophorin (Lp), either labeled in diacylglycerol moiety with [(3)H]-Palmitic acid or in phospholipid moiety with (32)Pi, was injected into Rhodnius prolixus females. Insects were induced to flight for different times. In just a few minutes of flight, the transfer of radioactivity to ovaries decreased, accompanied by its increase to flight muscles. After one hour of flight, Lp density was higher (1.132 g/mL) than before flight (1.116 g/mL). Lp purified from insects after flight was analyzed by gel filtration chromatography and a polyacrylamide gel pore limit electrophoresis. Both analyses demonstrated a decrease in Lp molecular mass after flight but no changes in apoLp-III amounts were observed. Time-course experiments showed that only 30 min of flight are required for the detection of changes in Lp density and molecular mass. About the same time of rest is necessary for Lp density and molecular mass to return to the baseline value. The lipid content from Lp particles, determined by high-performance thin-layer chromatography (HPTLC), showed a decrease in total lipids after flight. At the same time, an increase of many classes of lipids was observed in flight muscles except for triacylglycerol, which was reduced. The increase of flight muscle lipids was accompanied by a decrease of the ovaries lipid content. The insects subjected to daily exhaustive flight showed a significant decrease in total number of eggs produced. But insects subjected to a single exhaustive flight showed only a small reduction in total number of eggs. Lp density variation during the flight activity of Rhodnius prolixus females is discussed in association with physiological events such as oogenesis.