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The primary objective of this study was to investigate the pulmonary damage resulting from isolated or combined exposure to inhaled toluene (300 ppm) and noise 85 dB (A), with a focus on evaluating the potential protective effects of Olea europaea L. leaf extract (OLE). Forty-eight male Wistar rats were divided into eight groups: control (C), OLE treatment (O), noise exposure (N), noise exposure with OLE treatment (N+OLE), toluene exposure (T), toluene exposure with OLE treatment (T + OLE), co-exposure to toluene and noise (NT), and co-exposure with OLE treatment (NT + OLE). OLE (40 mg/kg/day) was administered daily for six weeks via oral gavage. Exposure to toluene and noise resulted in significant disruption of the pulmonary tissue structure, accompanied by oxidative stress, as evidenced by increased lipid peroxidation, diminished catalase and superoxide dismutase activities, and elevated pro-inflammatory cytokines IL6, IL-β, and TNF-α. Notably, the administration of OLE effectively mitigated oxidative stress and inflammation and preserved pulmonary histology. In conclusion, exposure to toluene and its combination with noise significantly elevated oxidative stress, inflammatory responses, and histological disruptions in the lung tissue. In contrast, noise exposure alone is characterized by minimal effects, although it is still associated with an inflammatory response. Notably, Olea europaea L. leaf extract (OLE) exhibits a substantial protective role, effectively mitigating the adverse effects of combined exposure and highlighting its potential as a therapeutic agent for lung health.

In this study, we aim to investigate the effect of industrial Olea europaea L. leaf extract (OLE) against bleomycin (BLM)-induced pulmonary fibrosis (PF) in rats. Male Wistar rats were treated with a single intratracheal injection of BLM (4 mg/kg) and a daily intraperitoneal injection of OLE (10, 20, and 40 mg/kg) for 4 weeks. Results of HPLC and LC-MS analysis revealed a large amount of oleuropein (15.43%/DW) in OLE. BLM induced apparent damage of lung architecture with condensed collagen bundles, increased lipid peroxidation which has been deduced from malondialdehyde (MDA) levels: (.9 ± .13 vs .25 ± .12 nmol/mg protein) and hydroxyproline content (.601 ± .22 vs .154 ± .139 mg/g of lung tissue) and decreased catalase (CAT) (5.93.10 −5 ± 4.23.10 −5 vs 6.41.10 −4 ± 2.33.10 −4 μmol/min/mg protein) and superoxide dismutase (SOD) (28.73 ± 3.34 vs 50.13 ± 2.1 USOD/min/mg protein) levels compared to the control. OLE treatment (40 mg/kg) stabilized MDA content (.32 ± .15 and .27 ± .13 vs .9 ± .13 nmol/mg protein), normalized SOD (61.27 ± 13.37 vs 28.73 ± 3.34 USOD/min/mg protein), and CAT (5.2.10 −4 ±1.8.10 −4 vs 5.93.10 −5 ± 4.23.10 −5 μmol/min/mg protein) activities and counteracted collagen accumulation and hydroxyproline content (.222 ± .07 vs .601 ± .22 mg/g of lung tissue) in the lung parenchyma. Finally, OLE might have a potent protective effect against PF by regulating oxidative parameters and attenuating collagen deposition, due to the existence of large amount of bioactive phenolic molecules.

In many occupational settings, workers are frequently exposed to toluene and noise. However, the individual and combined effects of these exposures on the cardiovascular system have not been fully elucidated. Therefore, this study aimed to investigate the impact of simultaneous exposure to toluene and noise on the rat heart, while also evaluating the potential preventive effect of olive leaf extract (OLE). Forty-eight male Wistar rats were randomly assigned to eight groups (n = 6/group): control group (C), control group that received OLE (C + OLE), group exposed to noise (N), group exposed to noise and receiving OLE (N + OLE), group exposed to toluene (T), group exposed to toluene and receiving OLE (T + OLE), group co-exposed to noise and toluene (NT), and group co-exposed to noise and toluene and receiving OLE (NT + OLE). The rats in this study were subjected to simultaneous exposure to toluene and noise for a duration of six weeks, within a custom-built plexiglass chamber. Toluene was administered at a concentration of 300 ppm, while the noise level was set to 85 dB(A). The exposure chamber was equipped with a generation system, an exposure system, and a monitoring system, ensuring precise and accurate exposure conditions. After the six-week period, heart and blood samples were collected from the rats for subsequent analysis. Plasma levels of cholesterol (CHOL), triglycerides (TG), lactate dehydrogenase (LDH), and creatine kinase (CK) were measured, and histopathological investigation was conducted using HE staining. Additionally, superoxide dismutase (SOD) and catalase (CAT) activities, as well as malondialdehyde (MDA) levels in heart tissue were measured. Our results showed that simultaneous exposure to noise and toluene altered CHOL, TG, LDH, and CK levels, and also caused an increase in lipid peroxidation levels and superoxide dismutase activity, along with a decrease in catalase activity in the heart. A significant alteration in the myocardium was also observed. However, treatment with OLE was found to modulate these oxidative and histological changes, ultimately correcting the deleterious effects induced by the combined exposure to noise and toluene. Therefore, our study suggests that OLE could be a potential preventive measure for individuals exposed to toluene and noise in industrial settings.