Oxidative stress in liver cell culture from mullet, Liza klunzingeri, induced by short-term exposure to benzo[a]pyrene and nonylphenol

In vitro effects of bisphenol F on antioxidant system indicators in the isolated hepatocytes of rainbow trout (Oncorhyncus mykiss)

“…In the present study, SOD activities were signi cantly increased with all of the BPF concentrations when compared to the control group, presumably in response to enhanced cellular superoxide anion radicals. In accordance with the present study, in vitro studies using sh hepatocytes have also reported increased SOD activities after exposure to different types of environmental chemicals, such as BPA [35], per uorinated organic compounds [29], di(2ethylhexyl) phthalate [36], and benzo[a]pyrene and nonylphenol [37]. On the other hand, no signi cant changes were seen in the SOD activity of juvenile common carp liver (Cyprinus carpio) samples after long-term (60 days) waterborne exposure to BPF [38].…”

“…Similar to these ndings, Maćczak et al found decreased levels of CAT in human erythrocytes treated with BPF for different periods of time (4 h and 24 h) [15]. Decreased CAT activity was also found in juvenile common carp [37], and the larvae of zebra sh after waterborne exposure to BPF [7]. Ullah et al, also reported that CAT activity was inhibited in the testicular tissues of rats exposed to BPF via drinking water [5].…”

Exposure to Benzo(a)pyrene Enhances Acetaminophen-Induced Liver Injury in Mice at Non-Hepatotoxic Doses

“…This is particularly worrisome as their mechanisms of action may coincide with that of APAP. Among these chemicals are the polycyclic aromatic hydrocarbons (PAHs), in particular benzo[a]pyrene (B[a]P), known for their capacity to induce oxidative stress [30][31][32]. Benzo[a]pyrene is considered a high-priority substance of concern for human exposure (8th/275), according to the Agency for Toxic Substances and Disease Registry [33].…”

“…Due to its lipophilicity, B[a]P is readily absorbed through biological membranes and undergoes bioactivation to reactive metabolites mediated by enzymes from the Cytochrome P450 (CYP) superfamily, including cytochrome P450 1A1 (CYP1A1), cytochrome P450 1A2 (CYP1A2), and cytochrome P450 1B1 (CYP1B1), resulting in the production of ROS and metabolites such as phenol forms, epoxides, dihydrodiols, dihydrodiol epoxides, and anti-7,8-dihydroxy-9,10-epoxy-7,8,9,10-tetrahydro-B[a]P [30,32,35,38,44,45]. It has been demonstrated that the production of B[a]P-7,8-epoxide, mediated by CYP1A1, and its subsequent transformation to B[a]P-trans-7,8-dihydrodiol (B[a]P-7,8-DHD) in the presence of epoxide hydrolase represent dangerous reactions, as B[a]P-7,8-DHD is converted to the carcinogenic metabolite 7β,8α-dihydroxy-9α,10α-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (BPDE), which creates DNA adducts, causing mutations and malignant transformations [35,46].…”

“…The cellular antioxidant system, including key enzymes such as superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), and non-enzymatic components like glutathione, plays a crucial role in eliminating or regulating the elevated levels of ROS produced in the body [30]. Despite this, some studies have demonstrated disturbances in antioxidant responses in the liver, lungs, kidneys, stomach, and brain induced by acute B[a]P treatment in a murine model [30,32].…”