Noise and toluene are among the numerous physical and chemical pollutants that can induce adverse effects on different body tissues and systems; nevertheless, most studies have only experimented the auditory changes induced by co-exposure to them. The present in-vivo study aimed to examine the endocrine effects of co-exposure to toluene and noise on the testes and adrenal glands. In this experimental study, 24 healthy male New Zealand White rabbits were used. The noise intensity was 100 dB (white noise) and the toluene concentration was 1000 ppm for two consecutive weeks. The luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, cortisol and adrenocorticotropic hormone (ACTH) were measured using the enzyme-linked immunosorbent assay (ELISA) method. The hematoxylin and eosin stain method (H&E) was performed for the histopathological analysis. Comparing different parameters in different groups on post-exposure days was carried out using GEE (generalized estimating equations) method. The results indicated that noise and toluene increased cortisol, LH and FSH levels during different days after the exposure. Exposure to toluene and noise made vacuolization and reduction of primary spermatogonial cells in the testes. Moreover, lymphocyte infiltration, congestion, swelling and vacuolization were detected in adrenal glands through exposure to toluene and noise. Toluene and noise induced different destructive effects on the endocrine system. More studies are required to elucidate other endocrine changes induced by exposure to toluene and noise.

In the present lifestyle, we are continuously exposed to radiofrequency electromagnetic field (RF-EMF) radiation generated mainly by mobile phones (MP). Among other organs, our brain and hippocampus in specific, is the region where effect of any environmental perturbation is most pronounced. So, this study was aimed to examine changes in major parameters (oxidative stress, level of pro-inflammatory cytokines (PICs), hypothalamic-pituitary-adrenal (HPA) axis hormones, and contextual fear conditioning) which are linked to hippocampus directly or indirectly, upon exposure to mobile phone radiofrequency electromagnetic field (MP-RF-EMF) radiation. Exposure was performed on young adult male Wistar rats for 16 weeks continuously (2 h/day) with MP-RF-EMF radiation having frequency, power density, and specific absorption rate (SAR) of 1966.1 MHz, 4.0 mW/cm², and 0.36 W/kg, respectively. Another set of animals kept in similar conditions without any radiation exposure serves as control. Towards the end of exposure period, animals were tested for fear memory and then euthanized to measure hippocampal oxidative stress, level of circulatory PICs, and stress hormones. We observed significant increase in hippocampal oxidative stress (p < 0.05) and elevated level of circulatory PICs viz. IL-1beta (p < 0.01), IL-6 (p < 0.05), and TNF-alpha (p < 0.001) in experimental animals upon exposure to MP-RF-EMF radiation. Adrenal gland weight (p < 0.001) and level of stress hormones viz. adrenocorticotropic hormone (ACTH) (p < 0.01) and corticosterone (CORT) (p < 0.05) were also found to increase significantly in MP-RF-EMF radiation-exposed animals as compared with control. However, alteration in contextual fear memory was not significant enough. In conclusion, current study shows that chronic exposure to MP-RF-EMF radiation emitted from mobile phones may induce oxidative stress, inflammatory response, and HPA axis deregulation. However, changes in hippocampal functionality depend on the complex interplay of several opposing factors that got affected upon MP-RF-EMF exposure.

This study investigated the role of melatonin (MLT) on adrenal gland toxicity induced by bisphenol A (BPA). Adult male rats were divided into four groups of seven animals each: Group I (control) received oral 0.2 ml canola oil; group II received intra-peritoneal 10 mg/kg BW/day MLT; and group III received oral BPA (10 mg/kg BW/day). Group IV rats were treated with same dose of BPA as group III with a concomitant intra-peritoneal 10 mg/kg BW/day MLT. All treatments lasted for 14 days. BPA significantly increased (P < 0.05) adrenal index, circulating levels of corticosterone and adrenocorticotropic hormone (ACTH) in the rats. BPA caused marked vascular congestion, hyperplasia, cellular distortion, increased lipid peroxidation, decreased antioxidant enzymes, and decreased expression of αSmooth muscle actin as well as vimentin proteins. The concomitant treatment with MLT ameliorated these BPA-induced alterations. It is likely that melatonin attenuates BPA-induced alterations of the adrenal gland of rats through the antioxidant defense mechanism.