The effects of radiofrequency electromagnetic fields (RF-EMF) on the control of body energy balance in developing organisms have not been studied, despite the involvement of energy status in vital physiological functions. We examined the effects of chronic RF-EMF exposure (900 MHz, 1 V m⁻¹) on the main functions involved in body energy homeostasis (feeding behaviour, sleep and thermoregulatory processes). Thirteen juvenile male Wistar rats were exposed to continuous RF-EMF for 5 weeks at 24 °C of air temperature (T ₐ) and compared with 11 non-exposed animals. Hence, at the beginning of the 6th week of exposure, the functions were recorded at T ₐ of 24 °C and then at 31 °C. We showed that the frequency of rapid eye movement sleep episodes was greater in the RF-EMF-exposed group, independently of T ₐ (+42.1 % at 24 °C and +31.6 % at 31 °C). The other effects of RF-EMF exposure on several sleep parameters were dependent on T ₐ. At 31 °C, RF-EMF-exposed animals had a significantly lower subcutaneous tail temperature (−1.21 °C) than controls at all sleep stages; this suggested peripheral vasoconstriction, which was confirmed in an experiment with the vasodilatator prazosin. Exposure to RF-EMF also increased daytime food intake (+0.22 g h⁻¹). Most of the observed effects of RF-EMF exposure were dependent on T ₐ. Exposure to RF-EMF appears to modify the functioning of vasomotor tone by acting peripherally through α-adrenoceptors. The elicited vasoconstriction may restrict body cooling, whereas energy intake increases. Our results show that RF-EMF exposure can induce energy-saving processes without strongly disturbing the overall sleep pattern.

This work aims to analyze the relationship between root growth, mitogen-activated protein kinase (MAPK), auxin signaling, and cell cycle-related gene expression in cadmium (Cd)-stressed rice. The role of MAPKs in auxin signal modification and cell cycle-related gene expression during root growth was investigated by disrupting MAPK signaling using the MAPKK inhibitor PD98059 (PD). Treatment with Cd caused a significant accumulation of Cd in the roots. A Cd-specific probe showed that Cd is mainly localized in the meristematic zone and vascular tissues. Perturbation of MAPK signaling using PD significantly suppressed root system growth under Cd stress. The transcription of six MAPK genes was inhibited by Cd compared to the control. Detection using DR5-GUS transgenic rice showed that the intensity and distribution pattern of GUS staining was similar in roots treated with PD or Cd, whereas in Cd plus PD-treated roots, the GUS staining pattern was similar to that of the control, which indicates a close association of MAPK signaling with auxin homeostasis under control and Cd stress conditions. The expression of most key genes of auxin signaling, including OsYUCCA, OsPIN, OsARF, and OsIAA, and of most cell cycle-related genes, was negatively regulated by MAPKs under Cd stress. These results suggest that the MAPK pathway plays specific roles in auxin signal transduction and in the control of the cell cycle in response to Cd stress. Altogether, MAPKs take part in the regulation of root growth via auxin signal variation and the modified expression of cell cycle-related genes in Cd-stressed rice. A working model for the function of MAPKs in rice root systems grown under Cd stress is proposed.

Perfluorinated compounds (PFCs) are a large group of chemicals used in different industrial and commercial applications. Studies have suggested the potential of some PFCs to disrupt endocrine homeostasis, increasing the risk of adverse health effects. This study aimed to elucidate mechanisms behind PFC interference with steroid hormone receptor functions. Seven PFCs [perfluorohexane sulfonate (PFHxS), perfluorooctane sulfonate (PFOS), perfluorooctanoate (PFOA), perfluorononanoate (PFNA), perfluorodecanoate (PFDA), perfluoroundecanoate (PFUnA), and perfluorododecanoate (PFDoA)] were analyzed in vitro for their potential to affect estrogen receptor (ER) and androgen receptor (AR) transactivity as well as aromatase enzyme activity. The PFCs were assessed as single compounds and in an equimolar mixture. PFHxS, PFOS and PFOA significantly induced the ER transactivity, whereas PFHxS, PFOS, PFOA, PFNA and PFDA significantly antagonized the AR activity in a concentration-dependent manner. Moreover, PFDA weakly decreased the aromatase activity at a high test concentration. A mixture effect more than additive was observed on AR function. We conclude that five of the seven PFCs possess the potential in vitro to interfere with the function of the ER and/or the AR. The observed mixture effect emphasizes the importance of considering the combined action of PFCs in future studies to assess related health risks.