Benzophenone-2 Concentration and Its Effect on Oxidative Stress and Apoptosis Markers in Rat Brain

Abstract

Benzophenones, frequently used as UV chemical filters, are absorbed through the skin and can exert systemic adverse effects. So far, most of the data are related to their action on sex hormone receptors whereas potential neurotoxic effect is expected mainly on the basis of in vitro studies. The aim of the present study was to determine concentrations of BP-2, oxidative stress and apoptosis markers in the rat brain after topical administration of this compound. Male Wistar rats were treated dermally with BP-2 (100 mg/kg, 4 weeks), and next, blood and tissue BP-2 concentrations and oxidative stress and apoptotic markers in the frontal cortex and hippocampus were determined. After dermal BP-2 administration, blood level of this compound was about 300 ng/ml while in the liver and adipose tissue 1354 and 823 ng/g wt tissue, respectively. In the studied brain structures, the levels of the test compound were from 5 to 19 ng/g tissue. In the hippocampus, where BP-2 level was about 3.5-fold lower than in the frontal cortex, no significant changes in either oxidative stress and apoptosis markers were observed. There was also no change in apoptosis markers in the frontal cortex but unexpectedly the oxidative stress markers were reduced. The research showed that BP-2 passes through the blood-brain barrier but its concentration in the brain structures are much lower than in the blood. This compound did not exacerbate oxidative stress and apoptosis markers in the hippocampus and frontal cortex, and even lowered oxidative stress in the frontal cortex.

Keywords: Benzophenone-2; Brain concentration; Oxidative stress; UV filters.

Fig. 1

A representative chromatogram of BP-2 standard (a) and serum of BP-2 treated rats without (b) and after (c) glucuronide and sulfate hydrolysis, and liver without (d) and after (e) hydrolysis

Fig. 2

Concentrations of free BP-2 in serum, liver, adipose tissue, cerebellum, frontal cortex, and hippocampus and total BP-2 concentrations after glucuronide and sulfate hydrolysis in serum and liver. Rats were treated dermally with 100 mg/kg BP-2 twice a day for 4 weeks and were killed 24 h after the last BP-2 application. Data are expressed as the means ± SEM and were statistically evaluated by one-way analysis of variance (ANOVA), followed by Duncan’s post hoc test. *p < 0.05 vs. control animals, n = 10

Fig. 3

The effect of BP-2 on reactive oxygen species (ROS) level in the frontal cortex and hippocampus, on total antioxidant capacity (TAC) in the frontal cortex and hippocampus and lipid peroxidation in the frontal cortex and hippocampus. Rats were treated dermally with 100 mg/kg BP-2 twice a day for 4 weeks and were killed 24 h after the last BP-2 application. Data are expressed as the means ± SEM and were statistically evaluated by one-way analysis of variance (ANOVA), followed by Duncan’s post hoc test. *p < 0.05 vs. control animals, n = 10