In this study, the effect of geraniol (50 mg/kg for 30 d), a natural antioxidant and repellent/antifeedant monoterpene, in a rat model of lead acetate-induced (500 ppm for 30 d) liver damage was evaluated. Hepatic malondialdehyde increased in the lead acetate group. Reduced glutathione unchanged, but glutathione S-transferase, glutathione reductase, as well as carboxylesterase activities decreased in geraniol, lead acetate and geraniol + lead acetate groups. 8-OhDG immunoreactivity, mononuclear cell infiltrations and hepatic lead concentration were lower in the geraniol + lead acetate group than the lead acetate group. Serum aspartate aminotransferase and alanine aminotransferase activities increased in the Pb acetate group. In conclusion, lead acetate causes oxidative and toxic damage in the liver and this effect can reduce with geraniol treatment. However, we first observed that lead acetate, as well as geraniol, can affect liver carboxylesterase activity.

Atatürk Dam Lake is one of the important freshwater ecosystems in the world in terms of the size of the surface area and the biodiversity. The objective of this study was to determine the effects of metal pollution in the Atatürk Dam Lake on some biochemical markers in the gills and digestive glands of mussels (Unio mancus). Mussel samples were collected in July-2018 from four stations. The metal residues (Cd, Cu, Pb, Zn, and Ni) in the tissues were determined by ICP-MS. The MT, reduced GSH, and MDA levels were analysed using the proposed spectrophotometric methods. According to the results, toxic metals such as Cd and Pb in both tissues were determined mostly in mussels collected from St1. The highest MT and MDA levels in the gills were determined in St3 and St2 respectively, while the highest MT and MDA levels in the digestive glands were determined in St1. Although there was no significant difference in the reduced GSH level in the gills among the stations, the highest reduced GSH level in the digestive glands was determined in St4. These results indicated that mussels are appropriate sentinel organisms for metal contamination with effects on oxidative stress and metal exposure biomarkers.

Background: Environmental pollution, including exposure to carbon tetrachloride (CCl4), poses serious health risks, particularly through oxidative stress, which may lead to neurodegenerative damage. Antioxidants, especially those found in natural products, show potential in mitigating these toxic effects. Pomegranate juice (PJ), rich in bioactive phytochemicals, has demonstrated antioxidant, anti-inflammatory, and neuroprotective properties.Objective: This study aimed to investigate the protective effects of PJ on neurotoxicity induced by CCl4 in rats, assessing specific markers of oxidative stress, enzymatic activity, and apoptotic cell death.Material and Methods: Twenty-eight male Wistar rats were divided into four groups: Control, CCl4, PJ, and CCl4+PJ. The CCl4 group received intraperitoneal injections of CCl4 (0.2 ml/100 g) twice weekly for six weeks, while the PJ group received PJ orally (4 ml/kg) daily for 30 days. The CCl4+PJ group received both treatments in sequence. Brain tissues were analysed for malondialdehyde (MDA), reduced glutathione (GSH), acetylcholinesterase (AChE), glutathione S-transferase (GST), glutathione reductase (GR), and carboxylesterase (CaE) activity. Apoptotic cell death was assessed using TUNEL staining.Results: CCl4 exposure resulted in a marked increase in MDA levels and AChE activity in brain tissue (p<0.05), alongside a significant decrease in reduced GSH levels and GST activity (p<0.05). Treatment with PJ significantly lowered MDA levels and AChE activity in the CCl4+PJ group compared to the CCl4 group (p<0.05). However, GSH levels and GST activity showed no significant changes in the CCl4+PJ group. TUNEL staining indicated a reduction in apoptotic cells in the CCl4+PJ group versus the CCl4 group, suggesting reduced cellular damage with PJ treatment (p<0.05).Conclusions: PJ demonstrates neuroprotective potential against CCl4-induced oxidative stress and neurotoxicity in rats by reducing oxidative markers and apoptosis. These findings suggest that PJ could serve as a natural protective agent against neurodegenerative risks associated with environmental pollutants like CCl4.