Benzene exposure causes structural and functional damage in rat ovaries: occurrence of apoptosis and autophagy.

Studies to date have provided evidence for damage that can occur from hydrocarbon benzene on different tissues/organs. However, little is known regarding the possible influence of this hydrocarbon on female reproduction. In this study, female Wistar rats were treated with low (2000 ppm), middle (4000 ppm), and high (8000 ppm) doses of benzene by inhalation for 30 min daily for 28 days. Benzene exposure adversely affected ovarian function and structure by inducing histopathological changes and altering reproductive steroid hormone release. In addition, benzene-exposed ovaries exhibited increased TMR red fluorescent signals at middle and high doses, revealing significant apoptosis. Interestingly, the investigation of the autophagic protein marker LC3 showed that this protein significantly increased in all benzene-treated ovaries, indicating the occurrence of autophagy. Moreover, ovaries from benzene-treated groups exhibited differential regulation of several specific genes involved in ovarian folliculogenesis and steroidogenesis, including the INSL3, CCND1, IGF-1, CYP17a, LHR, ATG5, and GDF9 genes.

High-fat diet-induced aggravation of cardiovascular impairment in permethrin-treated Wistar rats.

This study characterized the impact of post-weaning high-fat diet (HFD) and/or permethrin (PER) treatment on heart dysfunction and fibrosis, as well as atherogenic risk, in rats by investigating interactions between HFD and PER. Our results revealed that HFD and/or PER induced remarkable cardiotoxicity by promoting cardiac injury, biomarker leakage into the plasma and altering heart rate and electrocardiogram pattern, as well as plasma ion levels. HFD and/or PER increased plasma total cholesterol, triacylglycerols, and low-density lipoprotein (LDL) cholesterol levels but significantly reduced high-density lipoprotein (HDL) cholesterol. Cardiac content of peroxidation malonaldehyde, protein carbonyls, and reactive oxygen species were remarkably elevated, while glutathione levels and superoxide dismutase, catalase and glutathione peroxidase activities were inhibited in animals receiving a HFD and/or PER. Furthermore, cardiac DNA fragmentation and upregulation of Bax and caspase-3 gene expression supported the ability of HFD and/or PER to induce apoptosis and inflammation in rat hearts. High cardiac TGF-ß1 expression explained the profibrotic effects of PER either with the standard diet or HFD. Masson's Trichrome staining clearly demonstrated that HFD and PER could cause cardiac fibrosis. Additionally, increased oxidized LDL and the presence of several lipid droplets in arterial tissues highlighted the atherogenic effects of HFD and/or PER in rats. Such PER-induced cardiac and vascular dysfunctions were aggravated by and associated with a HFD, implying that obese individuals may be more vulnerable to PER exposure. Collectively, post-weaning exposure to HFD and/or PER may promote heart failure and fibrosis, demonstrating the pleiotropic effects of exposure to environmental factors early in life.