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The fine structure of the ventral intersegmental abdominal muscles of the insect Rhodnius prolixus during the molting cycle. II. Muscle changes in preparation for molting.

The development of the ventral intersegmental abdominal muscles of Rhodnius prolixus is triggered by feeding. The early muscle (1 day after feeding) contains essentially nonstriated fibrils. However, in cross-sections, areas indicating early I bands, Z lines, and A bands can be recognized. Interdigitating thick and thin myofilaments do not assemble into a precise lattice until sometime between 4 and 5 days after feeding. As development continues, the number of fibrils increases, the region corresponding to the Z line increases in density, and the fibrils contain more recognizable striations. The newly formed fibrils broaden as myofilaments are added peripherally. At all stages throughout development, the ratio of thin to thick myofilaments is always 6:1. The formation of fibrils in the abdominal muscles of Rhodnius is different from that in chick embryo skeletal muscle. The major differences are that at all stages in Rhodnius there are (1) a constant ratio of thin to thick myofilaments, and (2) detectable Z-line material. Other findings in Rhodnius suggest (1) that fusion of mononucleated cells with the multinucleated muscle cell occurs, (2) that microtubules develop in the tendon cell concomitantly with development of myofibrils in the associated muscle cell, and (3) that filaments 55A in diameter aggregate into microtubules.

Abdomen↗

The effect of pre- and postmolt diets high in n-3 fatty acids and molt programs on skeletal integrity and insulin-like growth factor-I of White Leghorns.

This study investigated changes in bone integrity and circulating concentrations of insulin-like growth factor-I (IGF-I) of hens subjected to 2 distinct molting regimens and fed pre- and postmolt diets high in n-3 or n-6 fatty acids. A dual-energy x-ray absorptiometer determined bone mineral density (BMD) of the tibia and humerus of 45 live hens from 62 to 76 wk of age. Densitometric scans were also conducted in excised tibia and humerus at 66, 71, and 76 wk of age. Concentrations of IGF-I were monitored using an homologous RIA at the same ages. The molting treatments consisted of 10 d of fasting + cracked corn for 7 d + pullet developer diet for 10 d or a nonfasting molt (wheat-middlings-based diet for 27 d). Five weeks prior to and after either molt treatment, birds were fed 1 of 2 diets containing dietary n-6/ n-3 fatty acids ratios of 0.6 or 8.0. At the end of the molt (71 wk of age), tibial BMD decreased 30% in fasted and 11% in nonfasted molt regimens, and the fatty acid content of the premolt diet had no effect on the decline in BMD. The BMD of the humerus also decreased during molt with the exception of hens subjected to a nonfasted molt and fed n-3 fatty acid diets in which their BMD values were similar to or greater (at 73 wk of age) than those of controls during the entire experimental period (treatment by bone by age, P < or = 0.0001). Induced molt affected circulating IGF-I concentrations (treatment by age interaction, P < or = 0.0001), and the response was the same regardless of molt regimen (fasting vs. nonfasting) or diet (n-3 vs. n-6 fatty acids). A decrease in IGF-I 54 h postmolt was noted; however, from 13 to 43 d postmolt, all molted birds had elevated IGF-I as compared with controls. In conclusion, a nonfasted molt as compared with fasted molt was less detrimental to bone mineralization; dietary n-6/n-3 fatty acid ratios in the pre- and postmolt diets had little effect on the decline of skeletal integrity during molt, and circulating IGF-I concentrations were affected by molt.

Aging↗

Mechanism of resistance to cyclopentenyl cytosine (CPE-C) in Molt-4 lymphoblasts.

Cyclopentenyl cytosine (CPE-C), a carbocyclic analogue of cytidine, has preclinical antineoplastic activity against ara-C resistant murine leukemias and a broad spectrum of human tumor xenografts. CPE-C is a prodrug and requires intracellular phosphorylation to cyclopentenyl cytosine triphosphate (CPE-CTP) which depletes endogenous CTP pools. The initial step in this activation process is catalyzed by uridine/cytidine kinase. We studied the mechanism of resistance to CPE-C in a Molt-4 T-cell leukemia line made resistant to CPE-C (Molt-4R) by culturing it in the continuous presence of increasing concentrations of CPE-C. Using a tetrazolium based colorimetric assay to assess cytotoxicity, the IC90 for the parent Molt-4 cells (Molt-4WT) was 0.5 microM after a 24 hr drug exposure. In contrast, cytotoxicity was not observed at concentrations as high as 1 mM in the Molt-4R cells. Following a brief exposure to 1 microM CPE-C, parent drug could be detected intracellularly in the resistant and sensitive cell lines. However, CPE-CTP formation was reduced markedly in the resistant cell line. Measurement of the activity of anabolic and catabolic enzymes in the Molt-4WT and Molt-4R cells revealed equivalent activities of alkaline and acid phosphatases as well as cytidine and dCMP deaminase but there was a significant reduction in uridine/cytidine kinase activity in Molt-4R cells. Endogenous ribonucleotide pools and CPE-CTP pools were measured in the absence and presence of CPE-C. CTP pools were reduced markedly in Molt-4WT cells following exposure to CPE-C. However, CTP pools in Molt-4R cells exposed to 100 microM CPE-C were two times greater than in the untreated Molt-4WT cells. At high concentrations of CPE-C (10 and 100 microM), Molt-4R cells were able to generate amounts of CPE-CTP equivalent to that seen in Molt-4WT cells exposed to 1 microM CPE-C (a cytotoxic concentration of drug in Molt-4WT cells), but no cytotoxic effect was seen in Molt-4R cells. Therefore, in addition to decreased uridine/cytidine kinase activity, a second mechanism of resistance that is the result of alterations in CTP synthetase activity also appears to be operative. Elucidation of the mechanism of resistance in vitro may provide insight into the mechanism of action of the drug and potential mechanisms of resistance in vivo.

Antineoplastic Agents↗

Thyroid and gonadal regulation of hair growth during the seasonal molt in the male European badger, Meles meles L.

In the male badger we showed that hair growth and molt are related to plasma testosterone and thyroxine cycles. We established the action of testosterone by castration and subcutaneous testosterone implants, and the action of thyroxine by thyroidectomy and dietary supplementation with thyroxine. The following groups of animals were studied: controls, thyroidectomized, thyroidectomized and thyroxine-treated, castrated, castrated and thyroxine-treated, thyroidectomized and castrated and thyroxine-treated, castrated and testosterone-implanted, and intact testosterone-implanted. In control animals, molt and hair growth occurred during the summer, with a maximum growth in autumn. Molt ended at the beginning of winter when the plasma testosterone level had started to rise, and began again after this level had started to decline. Both the start of molt and the period of maximum hair growth coincided with high thyroxine levels of about 20 ng/ml. Castration advanced molt and hair follicle activity, whereas testosterone implants delayed both molt and hair growth. In thyroidectomized badgers, neither hair growth nor seasonal molt was observed. However, when thyroxine levels were restored to 20 ng/ml or more by dietary T4 supplementation, molting was resumed in animals that had undergone either thyroidectomy or thyroidectomy plus castration. In those that underwent castration only, the molt was advanced leading to early hair growth further stimulated by the suppression of testosterone. Testosterone had an inhibitory effect on the molt--since testosterone implants in intact control animals delayed it by 4 weeks--but did not inhibit it completely. On the other hand, a T4-enriched diet advanced the date of the molt. However, the molt could not be induced, nor could hair follicle growth be reactivated, at all times during the annual cycle. Thus, in castrated animals. T4 enrichment of the diet in early January, at the end of the molt, caused follicle reactivation only toward the end of May, despite the lack of testosterone. This 18-week latency period from January to May might therefore constitute a "refractory period" in this species. The above findings show that the regulation of the seasonal molt and hair growth in the European badger involves both the thyroid and genital axes. This regulation is discussed in terms of joint control by the hypothalamus and pituitary governed, in turn, by an external factor--the photoperiod--considered to be the main synchronizer.

Animals↗

Control of molt in birds: association with prolactin and gonadal regression in starlings.

Despite the importance of molt to birds, very little is known about its environmental or physiological control. In starlings Sturnus vulgaris, and other species, under both natural conditions and experimental regimes, gonadal regression coincides with peak prolactin secretion. The prebasic molt starts at the same time. The aim of this series of experiments was to keep starlings on photo-schedules that would challenge the normally close relationship between gonadal regression and molt, to determine how closely the start of molt is associated with gonadal regression and/or associated changes in prolactin concentrations. In one series of experiments, photosensitive starlings were moved from a short photoperiod, 8 h light per day (8L), to 13 or 18L, and from 13 to 18L or 13 to 8L during testicular maturation. Later, photorefractory birds under 13L that had finished molting were moved to 18L. In another series of experiments, photorefractory starlings were moved from 18 to 8L for 7 weeks, 4 weeks, 2 weeks, 1 week, 3 days, 1 day, or 0 days, before being returned to 18L. There was no consistent relationship between photoperiod, or the increase in photoperiod, and the timing of the start of molt. Nor was there a consistent relationship with gonadal regression and the start of molt-molt could be triggered in the absence of a gonadal cycle. However, there was always an association between the start of molt and prolactin. In all cases where molt was induced, there had been an earlier increase in prolactin. However, the timing of molt was related to the time of peak prolactin, not the magnitude of that peak. This relationship between peak prolactin and the start of molt could explain the normally close relationship between the end of breeding activity and the start of molt.

Animals↗

Effect of induced molting on albumen quality, hatchability, and chick body weight from broiler breeders.

Commercial Cobb broiler breeders were subjected to molting from 55 to 62 wk of age. Incubating eggs were collected before molting and after molting and were stored for 18, 13, 8, or 3 d. Sample eggs were broken to measure albumen Haugh units (HU) and pH. Two hundred twenty-five eggs per treatment, stored for 18, 13, 8, or 3 d, were incubated for 21 d; the hatched chicks were weighed at the end of incubation and again after Day 7 of rearing. As the storage time increased, albumen HU decreased (P < 0.001). At all storage times, HU after molting were higher than those before molting (P < 0.001). Albumen pH increased with storage time (P < 0.001). A molting x storage interaction on pH was observed after 8 d of storage (P = 0.03). Hatchability of eggs increased after hens were molted, if the eggs were stored for a long time (P < 0.001). Body weights of 1-d-old chicks from the eggs of hens before molt were heavier than those from eggs after molting (P < 0.001). Conversely, at 7 d, the chicks from the eggs after molting were significantly heavier than those from eggs before molting (P < 0.001). We concluded that molting was a procedure to improve hatchability and chick juvenile growth. If eggs need to be stored, we recommended that fresh eggs with high HU value be stored rather than those with low HU values.

Aging↗

Effect of induced molting on the recurrence of a previous Salmonella enteritidis infection.

Previous work in the authors' laboratory had shown that hens infected with Salmonella enteritidis (SE) during the feed removal phase of an induced molt shed significantly more SE and more readily transmitted SE to uninfected hens in adjacent cages when compared with unmolted hens. A study was conducted to examine the effect of induced molting on the recurrence and horizontal transmission of a previous SE infection. Hens aged 59 and 69 wk in Trials 1 and 2, respectively, were infected with SE and then molted 21 days later. In Trial 1, more molted hens were SE-culture-positive on Days 38 (P < or = .005) and 45 (P < or = .005) postinfection, and these hens shed more SE on these days (P < or = .05 and P < or = .005, respectively) than unmolted hens. Horizontal transmission of SE to previously uninfected but contact-exposed hens in adjacent cages was also higher in the molted group than the unmolted group on Days 38 (P < or = .05) and 45 (P < or = .001). Molted, contact-exposed hens also shed significantly more SE than unmolted hens. In Trial 2, the molted infected hens shed progressively more SE than the unmolted hens but the differences were not significant. However, more molted contact-exposed hens became SE-positive at Day 31 (P < or = .05) and 38 (P < or = .005) and also shed more SE on these days (P < or = .05 and P < or = .01), respectively) than the unmolted hens. Serum and intestinal antibody titers to SE were also examined in Trial 2. Molting appeared to exert no effect on the serum SE titers, but antibody titers in the alimentary tract were lower in the molted hens than the unmolted hens on Days 45 (P < or = .005) and 52 (P < or = .05). In Trial 1, three of eight molted directly infected hens and two of eight molted contact-exposed hens produced any SE-contaminated eggs. In Trial 2, no SE-contaminated eggs were produced.

Animals↗

Effect of two different molting procedures on a Salmonella enteritidis infection.

Previous studies have shown that inducing a molt using feed removal exacerbated an intestinal infection by Salmonella enteritidis (SE). The current study was conducted to determine whether inducing a molt using a molt diet would still cause a pause in egg laying but not exacerbate an intestinal SE infection. In Experiments 1 and 2, hens were either provided ad libitum access to layer feed (control), fed 45 g molt diet (molt-feed) daily, or deprived of feed for 14 d (molted), and were orally infected with 1 x 10(7) SE on Day 4 of molt. Egg lay ceased in hens subjected to both molt treatments. The percentage of hens shedding SE did not differ among treatment groups in Experiment 1, whereas in Experiment 2 the molted hens had significantly higher shed rates than the controls on Days 10, 17, and 24 postinfection and the molt-feed hens on Days 17 and 24 postinfection. Compared with both fed groups of hens, the molted hens shed significantly more SE in Experiment 1 on Day 10 postinfection, and in Experiment 2 the molted hens shed significantly more SE on all 4 sampling days. In Experiment 3, subgroups of hens within each treatment group received serial 10-fold dilutions of SE and intestinal shedding of the organism in each subgroup was determined 7 d later. The 50% infectious dose (ID50) was calculated for each treatment group from these shedding results.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Dietary thyroxine induces molt in chickens (Gallus gallus domesticus).

Thyroxine increases during a molt in wild and captive birds, and thyroidectomy prevents induction of molt. This trial examined the effect of dietary thyroxine on molt induction molt in chickens (laying hens, 59 weeks of age). In a completely randomized design (n=15 hens/replication; 6 replications/treatment), hens were randomly assigned to either a traditional molting program consisting of feed withdrawal (FWD), or to diets containing 40 mg thyroxine/kg diet (HT), 20 mg thyroxine/kg diet (LT), or 40 mg thyroxine from thyroactive iodinated casein/kg diet (TIC). The molting treatment lasted 7-13 d, until egg production reached 0%. After molt induction, birds had ad libitum access to the same diet, until egg production was re-initiated and maximized ( approximately 56 d). All treatments induced molt, based upon cessation of egg laying and regression of ovary and oviduct. Birds on FWD treatment lost more body weight during the molting period, but gained more after molt compared to thyroxine treatments (P<0.01 for each), although all body weights were similar when egg production was maximized. Data demonstrate that oral thyroxine, in purified or non-purified form, induces a molt and may enhance animal well-being by reducing the need for FWD.

Animals↗

Hormonal correlations at transition from reproduction to molting in an annual life cycle of Humboldt penguins (Spheniscus humboldti).

To understand the hormonal mechanism behind a unique strategy of breeding and molting in Humboldt penguins, six pairs of captive Humboldt penguins kept in an outdoor open display pen were observed and blood collected weekly for a year. They all molted between the middle of June and the middle of August within 10 days except one pair that molted about a month later. The late pair had been rearing a hatchling until July due to the successful second clutch after the first clutch failed. A peak of plasma levels of thyroxine and triiodothyronine, respectively, overlapped a period of molting in both sexes. Plasma testosterone concentrations in the males and females were lowest for two month during a period of pre-molt and molting. Plasma concentrations of estradiol were also lowest during the molt in both sexes. Except for the period of molting, sex steroid hormone concentrations were high although there was great individual variation. During the molt, the birds were forced to fast since they did not enter the pool in the display pen where they usually forage live fish. To compensate this forced fasting, they took more food than usual during pre-molting period and gained body mass to about 20% more than the baseline value. Increased flipper thickness was parallel to increased body mass indicating that the gained body mass attributed to fat reservoir. These data indicate that rapid molting in Humboldt penguins is correlated with a drastic increase and decrease of thyroid hormones during the period of lowest concentrations in sex steroid hormones.

Animals↗

Effect of age at molting on postmolting performance.

Molt was induced at the 431, 501, or 571 d, in Lohmann (L) and Hy-Line W-77 (H) hens, by 8 or 14 d, respectively, of feed withdrawal followed by a rest period of 16 d. Induced molt resulted in increases in egg production, numbers of intact eggs, egg mass per housed or surviving hen, and shell quality and in decreases in egg breakage (not significant), mortality, and culling. Egg weight was only slightly affected by molt, and the EW of hens induced to molt at 431 or 501 d of age were slightly lower than those of the unmolted hens or of those induced to molt at 571 d. Both strains reacted similarly to molt, although the L hens responded better, and expressed their responses more intensively when induced to molt earlier (431 d). This finding suggests that although different breeds have some effects of molt in common, molt protocols should be finely tuned for each breed. Total intact egg production and egg mass of the molted hens became higher than those of the unmolted hens at 650 to 728 d, which suggests that no benefit would be achieved by rearing molted hens for less than 700 to 730 d.

Aging↗