Maternal Reproductive Toxicity of Some Essential Oils and Their Constituents

Even though several plants can improve the female reproductive function, the use of herbs, herbal preparations, or essential oils during pregnancy is questionable. This review is focused on the effects of some essential oils and their constituents on the female reproductive system during pregnancy and on the development of the fetus. The major concerns include causing abortion, reproductive hormone modulation, maternal toxicity, teratogenicity, and embryo-fetotoxicity. This work summarizes the important studies on the reproductive effects of essential oil constituents anethole, apiole, citral, camphor, thymoquinone, trans-sabinyl acetate, methyl salicylate, thujone, pulegone, β-elemene, β-eudesmol, and costus lactone, among others.

Degenerate circuits use distinct mechanisms to respond similarly to the same perturbation

There is considerable flexibility embedded within neural circuits. For example, separate modulatory inputs can differently configure the same underlying circuit but these different configurations generate comparable, or degenerate, activity patterns. However, little is known about whether these mechanistically different circuits in turn exhibit degenerate responses to the same inputs. We examined this issue using the crab (Cancer borealis) stomatogastric nervous system, in which stimulating the modulatory projection neuron MCN1 and bath applying the neuropeptide CabPK II elicit similar gastric mill (chewing) rhythms in the stomatogastric ganglion, despite differentially configuring the same neural circuit. We showed previously that bath applying the peptide hormone CCAP or stimulating the muscle stretch-sensitive sensory neuron GPR during the MCN1-elicited gastric mill rhythm selectively prolongs the protraction or retraction phase, respectively. Here, we found that these two influences on the CabPK-rhythm elicited some unique and unexpected consequences compared to their actions on the MCN1-rhythm. For example, in contrast to its effect on the MCN1-rhythm, CCAP selectively decreased the CabPK-rhythm retraction phase and thus increased the rhythm speed, whereas the CabPK-rhythm response to stimulating GPR during the retraction phase was similar its effect on the MCN1-rhythm (i.e. prolonging retraction). Interestingly, despite the comparable GPR actions on these degenerate rhythms, the underlying synaptic mechanism was distinct. Thus, degenerate circuits do not necessarily exhibit degenerate responses to the same influence, but when they do, it can occur via different underlying mechanisms.Significance StatementCircuits generating seemingly identical behaviors are often thought to arise from identical circuit states, as that is the most parsimonious explanation. Here we take advantage of an alternate scenario wherein a well-defined circuit with known connectivity generates similar activity patterns using distinct circuit states, via known mechanisms. The same peptide hormone modulation of these distinct circuit states produced divergent activity patterns, whereas the same sensory feedback altered these circuit outputs similarly but via different synaptic pathways. The latter observation limits the insights available from comparable studies in systems lacking detailed access to the underlying circuit.

Epigenetic Modifications due to Environment, Ageing, Nutrition, and Endocrine Disrupting Chemicals and Their Effects on the Endocrine System

The epigenome of an individual can be altered by endogenous hormones, environment, age, diet, and exposure to endocrine disrupting chemicals (EDCs), and the effects of these modifications can be seen across generations. Epigenetic modifications to the genome can alter the phenotype of the individual without altering the DNA sequence itself. Epigenetic modifications include DNA methylation, histone modification, and aberrant microRNA (miRNA) expression; they begin during germ cell development and embryogenesis and continue until death. Hormone modulation occurs during the ageing process due to epigenetic modifications. Maternal overnutrition or undernutrition can affect the epigenome of the fetus, and the effects can be seen throughout life. Furthermore, maternal care during the childhood of the offspring can lead to different phenotypes seen in adulthood. Diseases controlled by the endocrine system, such as obesity and diabetes, as well as infertility in females can be associated with epigenetic changes. Not only can these phenotypes be seen in F1, but also some chemical effects can be passed through the germline and have effects transgenerationally, and the phenotypes are seen in F3. The following literature review expands upon these topics and discusses the state of the science related to epigenetic effects of age, diet, and EDCs on the endocrine system.

Attenuation of satiety gut hormones increases appetitive behavior after curative esophagectomy for esophageal cancer

ABSTRACT Background Reduced appetite and weight loss are common after esophagectomy (ES), and this cohort demonstrates an exaggerated postprandial satiety gut hormone response. Satiety gut hormones modulate food reward, resulting in reduced energy intake. Objectives This study aimed to determine the effect of satiety gut hormone modulation by measuring the effect of the somatostatin analog octreotide on appetitive behavior among patients after ES. Methods In this randomized, double-blind, placebo-controlled crossover study, patients ≥1 y after ES and matched controls received either 1 mL 0.9% saline or 1 mL (100 μg) octreotide subcutaneously before completing a progressive ratio task. A measure of appetitive behavior, this task requires subjects to undertake progressively increasing amounts of work to obtain a sweet-fat reinforcer; the final completed increment (breakpoint) represents reinforcer reward value. Separate cohorts were studied in the fasted or 1-h postprandial states. Results Thirty-six subjects (ES, n = 18; matched controls, n = 18) were studied. The ES subjects were 2.5 ± 0.3 y postoperation and had a weight loss of 14.6% ± 2.6% and elevated postprandial glucagon-like peptide 1 compared with controls (49.2 ± 13.4 compared with 20.2 ± 2.3 pM; P = 0.04). Octreotide did not alter the breakpoint among ES or control subjects when tested in a fasting condition (ES: 980 ± 371 compared with 1700 ± 584 clicks; P = 0.16; controls: 1056 ± 274 compared with 1124 ± 273 clicks; P = 0.81). When tested 1 h postprandially, octreotide was associated with an increased breakpoint compared with placebo among ES subjects (322 ± 143 compared with 246 ± 149 clicks; P = 0.04) but not controls (248 ± 119 compared with 247 ± 120 clicks; P = 0.97). Conclusions Attenuation of the exaggerated postprandial satiety gut hormone response is associated with increased appetitive behavior toward a sweet-fat stimulus among patients post-ES. Suppression of satiety gut hormones may be a novel target to increase appetite, food intake, and body weight among patients after ES. This study was registered at clinicaltrials.gov as NCT02381249.

Effect of hormone modulation therapy on bone tissue in the treatment of endometriosis

This article presents a review of the current literature on the impact of such drugs as gonadotropin-releasing hormone agonists, aromatase inhibitors, and dienogest 2 mg, which are used for the treatment of external genital endometriosis, on the mineral density state. In the paper, we discuss the pathogenetic mechanisms of the effects of various bioactive compounds on bone and the results of domestic and foreign research.