Reproductive Suicide: Similar Mechanisms of Aging in C. elegans and Pacific Salmon

In some species of salmon, reproductive maturity triggers the development of massive pathology resulting from reproductive effort, leading to rapid post-reproductive death. Such reproductive death, which occurs in many semelparous organisms (with a single bout of reproduction), can be prevented by blocking reproductive maturation, and this can increase lifespan dramatically. Reproductive death is often viewed as distinct from senescence in iteroparous organisms (with multiple bouts of reproduction) such as humans. Here we review the evidence that reproductive death occurs in C. elegans and discuss what this means for its use as a model organism to study aging. Inhibiting insulin/IGF-1 signaling and germline removal suppresses reproductive death and greatly extends lifespan in C. elegans, but can also extend lifespan to a small extent in iteroparous organisms. We argue that mechanisms of senescence operative in reproductive death exist in a less catastrophic form in iteroparous organisms, particularly those that involve costly resource reallocation, and exhibit endocrine-regulated plasticity. Thus, mechanisms of senescence in semelparous organisms (including plants) and iteroparous ones form an etiological continuum. Therefore understanding mechanisms of reproductive death in C. elegans can teach us about some mechanisms of senescence that are operative in iteroparous organisms.

The insect somatostatin pathway gates vitellogenesis progression during reproductive maturation and the post-mating response

Oogenesis is closely linked with reproductive maturation and mating status in females. In the fruit fly Drosophila melanogaster, vitellogenesis (yolk accumulation) is an important control point for oogenesis. Vitellogenesis begins upon eclosion and continues through the process of sexual maturation. Upon reaching sexual maturity, vitellogenesis is placed on hold until it is induced again by a mating signal. In flies, this mating signal is sex peptide (SP), a seminal substance that triggers robust egg-laying activity. However, the neural mechanisms that gate vitellogenesis in response to developmental and reproductive signals remain unclear. Here, we have identified a pair of thoracic ganglion neurons that produce the neuropeptide allatostatin C (AstC-mTh). AstC inhibits the biogenesis of juvenile hormone (JH), a key endocrine stimulator of vitellogenesis. Our genetic evidence indicates that AstC-mTh neurons gate both the initiation of vitellogenesis that occurs post-eclosion and its re-initiation post-mating. During sexual maturation, which takes place shortly after eclosion, AstC-mTh neurons are activated by excitatory inputs from SP abdominal ganglion (SAG) neurons. In mature virgin females, high sustained activity of SAG neurons seems to shut off vitellogenesis via continuous activation of the AstC-mTh neurons. Upon mating, however, SP inhibits SAG neurons, leading to AstC-mTh neuronal activation. As a result, the inhibition of the CA maintained by the AstC neurons is lifted. This permit both JH biosynthesis and the progression of vitellogenesis in mated females. Our work has uncovered a central neural circuit that gates the progression of oogenesis during sexual maturation and the post-mating response.

Timing the Juvenile-Adult Neurohormonal Transition: Functions and Evolution

Puberty and metamorphosis are two major developmental transitions linked to the reproductive maturation. In mammals and vertebrates, the central brain acts as a gatekeeper, timing the developmental transition through the activation of a neuroendocrine circuitry. In addition to reproduction, these neuroendocrine axes and the sustaining genetic network play additional roles in metabolism, sleep and behavior. Although neurohormonal axes regulating juvenile-adult transition have been classically considered the result of convergent evolution (i.e., analogous) between mammals and insects, recent findings challenge this idea, suggesting that at least some neuroendocrine circuits might be present in the common bilaterian ancestor Urbilateria. The initial signaling pathways that trigger the transition in different species appear to be of a single evolutionary origin and, consequently, many of the resulting functions are conserved with a few other molecular players being co-opted during evolution.

AN AYURVEDIC OVERVIEW OF RAKTAPRADAR- A CONCEPTUAL APPROACH

Reproductive capability in a young woman begins at the point of menarche, which is the beginning of cyclic uterine bleeding in the anatomically and physiologically normal female. Menarche marks the beginning of an important stage in a young woman’s physical reproductive maturation and development. Even before the onset of this entirely natural but potentially disturbing function, a young woman’s early psychological reactions to menstruation, and probably also her lifelong view, can be influenced by the accuracy of her information and the degree of empathy with which this knowledge has been conveyed to her. Many women, perhaps appropriately, conclude that any departure from their personal menstrual experience is abnormal, and they will seek treatment for these departures. Conversely, some women accept or perhaps ignore even significant variations in their menstrual function, sometimes to the extent that serious health impairment occurs (e.g., severe iron-deficiency anemia). Therefore in this study an effort has been put forth to make a conceptual study covering almost all the aspect of Raktapradar as per Ayurvedic and modern.

Semelparity and Reproductive Death in Caenorhabditis elegans

In some species of salmon, reproductive maturity triggers the development of massive pathology resulting from reproductive effort, leading to rapid post-reproductive death. Such reproductive death, which occurs in many semelparous organisms (with a single bout of reproduction), can be prevented by blocking reproductive maturation, and this can increase lifespan dramatically. Reproductive death is often viewed as distinct from senescence in iteroparous organisms (with multiple bouts of reproduction) such as humans. Here we review the evidence that reproductive death occurs in C. elegans and discuss what this means for its use as a model organism to study aging. Inhibiting insulin/IGF-1 signaling and germline removal suppresses reproductive death and greatly extends lifespan in C. elegans, but can also extend lifespan to a small extent in iteroparous organisms. We argue that mechanisms of senescence operative in reproductive death exist in a less catastrophic form in iteroparous organisms, particularly those involving costly resource reallocation, and exhibiting endocrine-regulated plasticity. Thus, mechanisms of senescence in semelparous organisms (including plants) and iteroparous ones form an etiological continuum. Therefore understanding mechanisms of reproductive death in C. elegans can teach us about some mechanisms of senescence that are operative in iteroparous organisms.

Carotenoid feed supplementation in Argentine penaeoid shrimp broodstock

This work aimed to improve reproductive maturation in two penaeoid species (Artemesia longinaris and Pleoticus muelleri) by using carotenes added in artificial feeds and comparing antioxidant activity and carotenoids profiles. Immature females were kept for 45 days at salinity 33, temperature at 18°C, pH 7, 12:12 h photoperiod, ammonium <0.2mg L-1 and seawater exchanged at 100% per day. Feeding regimes consisted of 50% fresh frozen ingredients (clam muscle and squid mantle) and 50% dry pellets. For each species, three pelletized feeds were tested, one as a control (C) and two supplemented each one with 300 mg astaxanthin (A) and β-carotene (B) kg-1 of diet. At the end of the trials, ovaries, midgut gland, and integument were sampled. In both species, the addition of carotenoids improved ovarian development: 100% of females fed A or B diets were mature, but of the females fed with diet C only 75% (P. muelleri) and 64% (A. longinaris) matured. Ovaries of mature females exhibited the highest concentration of carotenoids. The abundance of free astaxanthin regarding total carotenes, suggests that excess of free astaxanthin could be biotransformed to esterified astaxanthin. The scavenging properties were evaluated against the stable 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical by electron resonance spectroscopy (EPR). For all feed treatments, the extracts exhibited strong DPPH scavenging activity, without significant differences among them.

Anthropogenic food enhancement alters the timing of maturational landmarks among wild savanna monkeys (Chlorocebus pygerythrus)

ABSTRACTAnthropogenic landscapes are rapidly replacing natural nonhuman primate habitats. Yet, the access to anthropogenic resources on primate biology, health, and fitness remain poorly studied. Given their ubiquity across a range of human impacted landscapes, from cities to national parks, savanna monkeys (Chlorocebus spp.) provide an excellent study system in which to test these effects. We compared body condition and reproductive maturation in vervets (Chlorocebus pygerythrus) inhabiting a private farm in !Gariep Dam, with ample access to anthropogenic foods, and wild-foraging vervets in Soetdoring Nature Reserve, South Africa. Overall, vervets in !Gariep show significantly thicker skin folds, and higher BMI and body mass, than those in Soetdoring, suggesting increased fat deposition. Males in !Gariep have larger relative testis volumes at peri-pubescent ages compared to those in Soetdoring, suggesting early reproductive maturation associated with age-specific increases in body mass. Females from !Gariep showed evidence of an earlier onset of reproduction than those in Soetdoring, based on parity status as assessed by nipple length and evidence of lactation. Parity status at sub-adult dental ages was also strongly associated with body mass. These results are consistent with a positive effect of anthropogenic food-enhancement on body fat deposition, potentially linked to an earlier onset of reproductive maturation. Further investigation into primate responses to cultivated resources will inform our understanding of the broader effects of food enhancement on developmental plasticity.