BDE-85 is a congener of a class of flame-retardant compounds called polybrominated diphenyl ethers (PBDEs). Although there are some studies on other congeners of PBDEs, there are none on the toxicity potential of this penta-BDE member. This study, therefore, reports the oxidative status and sciatic nerve conduction properties following BDE-85 treatment in rodents. The oxidative stress markers, lipid hydroperoxides, and the activities of antioxidant enzymes, namely superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione-S-transferase (GST), and catalase, in the exposed mice liver and brain tissues showed tissue-specific alterations following intraperitoneal injection of 0.25 mg/kg body weight of BDE-85 for 4 days. The results indicate a significant disruption in the oxidant/antioxidant equilibrium and setting in of oxidative stress. Isolated sciatic nerves of rats exposed to 5 µg/mL or 20 µg/mL of BDE-85 showed a significant reduction in nerve conduction velocity and compound action potential amplitudes, indicating physiological damage to the sciatic nerves.

Brominated flame retardants (BFRs) are synthetic organobromide compounds which inhibit ignition and combustion processes. Because of their immense ability to retard fire and save life and property, they have been extensively used in many products such as TVs, computers, foam, plastics etc. The five major classes of BFRs are tetrabromobisphenol-A (TBBPA), hexabromocyclododecane (HBCD), pentabromodiphenyl ether, octabromodiphenyl ether, and decabromodiphenyl ether. The last three are also commonly called PBDEs. BDE-85 and BDE-209 are the two prominent congeners of PBDEs and this study reports the adverse effects of these congeners in rodents. Exposure of rat sciatic nerves to 5 μg/mL and 20 μg/mL of BDE-85 and BDE-209 respectively lead to significant, concentration dependent reduction in nerve conduction function. Glucose absorption in the rat intestinal segments exposed to 5 μg/mL of BDE-85 and BDE-209 was significantly reduced for both the compounds tested. Lastly, mice when exposed to 0.25 mg/kg body weight for four days showed a disruption in oxidant and antioxidant equilibrium. The tissues namely liver and brain have shown increase in the levels of lipid hydroperoxides indicating oxidative stress. Moreover, all the protective enzymes namely superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase, and glutathione S transferase (GST) have shown tissue specific alterations indicating the induction of damaging oxidative stress and setting in of lipid peroxidation in exposed animals. The results indicate monitoring of PBDEs in the environment is essential because levels as low as 5 μg/mL and 0.25 mg/kg body weight were able to cause damage to the functions of rodents.

The Polybrominated Diphenyl Ethers (PBDEs) are a class of synthetic flame retardant compounds which are available in three commercial forms, penta BDEs, octa BDEs, and deca BDEs. Because of their extensive commercial use they have become widespread environmental contaminants. BDE-85 is a congener of the penta variety; to the best of the authors' knowledge there are no studies reported on the toxicity potential of this compound. This study reports the effects of BDE-85 on the oxidative stress and glucose absorption in rodents. Oxidative stress was measured using oxidative stress markers, lipid hydroperoxides in conjunction with activities of antioxidant enzymes, superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione-S-transferase (GST), and catalase in mice kidney and intestine tissues after exposure to 0.25 mg/kg body weight of BDE-85 via intraperitoneal route for four days. Mice tissues showed significant alterations (p<0.05) in the oxidative stress markers. Lipid hydroperoxide levels were elevated, indicating increased lipid peroxidation, while the activities of GPx, SOD, catalase and GST were reduced despite increased lipid peroxidation pointing to disruption in oxidant/antioxidant equilibrium. In addition to this, glucose absorption and Na+/K+ ATPase activities were studied in rats using isolated small intestinal segments exposed to 5 μg/mL of BDE-85 in vitro. The results showed a significant reduction (-63.97%) in the absorption of glucose through the small intestine along with decreased Na+/K+ ATPase activity, indicating significant disruption in the sodium-dependant glucose absorption process in the small intestine.