The disruption of circadian rhythms by environmental conditions can induce alterations in body homeostasis, from behavior to metabolism. The light:dark cycle is the most reliable environmental agent, which entrains circadian rhythms, although its credibility has decreased because of the extensive use of artificial light at night. Light pollution can compromise performance and health, but underlying mechanisms are not fully understood. The present review assesses the consequences induced by constant light (LL) in comparison with dim light at night (dLAN) on the circadian control of metabolism and behavior in rodents, since such an approach can identify the key mechanisms of chronodisruption. Data suggest that the effects of LL are more pronounced compared to dLAN and are directly related to the light level and duration of exposure. Dim LAN reduces nocturnal melatonin levels, similarly to LL, but the consequences on the rhythms of corticosterone and behavioral traits are not uniform and an improved quantification of the disrupted rhythms is needed. Metabolism is under strong circadian control and its disruption can lead to various pathologies. Moreover, metabolism is not only an output, but some metabolites and peripheral signal molecules can feedback on the circadian clockwork and either stabilize or amplify its desynchronization.

Circadian rhythms control almost all aspects of physiology and behavior, allowing temporal synchrony of these processes between each other, as well as with the external environment. In the immune system, daily rhythms of leukocyte functions can determine the strength of the immune response, thereby regulating the efficiency of defense mechanisms to cope with infections or tissue injury. The natural light/dark cycle is the prominent synchronizing agent perceived by the circadian clock, but this role of light is highly compromised by irregular working schedules and unintentional exposure to artificial light at night (ALAN). The primary concern is disrupted circadian control of important physiological processes, underlying potential links to adverse health effects. Here, we first discuss the immune consequences of genetic circadian disruption induced by mutation or deletion of specific clock genes. Next, we evaluate experimental research into the effects of disruptive light/dark regimes, particularly light-phase shifts, dim ALAN, and constant light on the innate immune mechanisms under steady state and acute inflammation, and in the pathogenesis of common lifestyle diseases. We suggest that a better understanding of the mechanisms by which circadian disruption influences immune status can be of importance in the search for strategies to minimize the negative consequences of chronodisruption on health.

In many animal species, embryos are exposed to maternal hormones that affect their development. Maternal hormone transfer varies with environmental conditions of the mother and is often interpreted as being shaped by natural selection to adjust the offspring to prevailing environmental conditions. Such hormone transfer requires genetic variability, which has not yet been experimentally demonstrated. Our study reports direct evidence for additive genetic variance of maternal androgens through a bidirectional selection on yolk testosterone (T) levels in Japanese quail. Lines selected for high egg T (HET) and low egg T (LET) concentration differed in yolk levels of this androgen, resulting in high realized heritability (h² = 0.42)Correlated responses to selection on other gonadal hormones indicated that selection specifically targeted biologically active androgens. Eggs of HET quail contained higher androstenedione and lower estradiol concentrations than did those of LET quail, with no line differences in yolk progesterone concentration. Plasma T concentrations in adult females were not affected by selection, seriously challenging the hypothesis that transfer of maternal hormones to offspring is constrained by hormone levels in a mother's circulation. Our results suggest that transfer of maternal T represents an indirect genetic effect that has important consequences for the evolution of traits in offspring.

The aim of our study was to investigate effects of increased testosterone content in egg yolk on early behaviour of 1- and 2-day-old Japanese quail. Three different doses of testosterone (0.25; 2.5 and 25 ng), not exceeding a physiological range, were examined in three separate experiments. Testosterone propionate dissolved in 20 μl olive oil was injected into the yolk before the onset of incubation. Behaviour of newly hatched chicks was recorded in response to both a novel environment in the open-field test and manual restraining in the test of tonic immobility (TI). Behavioural consequences of embryonic exposure to elevated testosterone were observed in the open-field test in all three experiments which indicated inhibition of behavioural responses in hatchlings. Birds treated with testosterone in ovo displayed longer latency to leave the start square, decreased locomotor activity, enhanced defecation and lower number of distress calls as compared to control birds. In TI test, the influence of treatment was manifested at the highest concentration only. Hatchlings from testosterone treated eggs expressed longer duration of TI and required less attempts to induce TI in comparison with the control group. Our results demonstrated increased fearfulness of Japanese quail chicks hatched from eggs with experimentally elevated testosterone content. The effect is specific for a short period after hatching since previous studies reported stimulatory effect of yolk testosterone on behaviour of Japanese quail later in ontogeny.