Pulmonary apoptotic and oxidative damaging effects of Triclosan alone or in combination with Fluoride in Sprague Dawley rats.

Research paper by Amany Tharwat AT Mohammed, Amany Abdel-Rahman AA Mohamed, Haytham H Ali

Indexed on: 04 Apr '17Published on: 04 Apr '17Published in: Acta Histochemica


This study aimed to assess the potential apoptotic and oxidative damaging impacts of Triclosan (TCS) and Sodium Fluoride (NaF) administered separately or in combination, in rats for thirty days. For this purpose, forty immature female Sprague-Dawley rats were equally allocated into five groups. TCS group administered 185mg TCS/kg Bw dissolved in distilled water (DW), while its control group received only DW. NaF group was given 50mg/kg NaF in corn oil BW and its respective control had corn oil alone. The co-treated group was administered TCS and NaF. The oxidative stress biomarkers were evaluated in lung tissue homogenate and apoptotic proteins (BcL-2 and Caspase-3) expression were quantified in lung tissues. The results of TCS or NaF treated groups revealed a prominent depletion of super oxide dismutase (SOD), Catalase (CAT) and Glutathione (GSH) in lung tissue homogenate. On contrary, a marked increase in the tissue levels of Malondialdehyde (MDA) and lactate dehydrogenase (LDH) enzymatic assay levels. The co-exposed group evoked less severity in the oxidative stress biomarkers concentration than individually exposed groups. The apoptotic genes protein expression was significantly higher in TCS or NaF treated rats when compared to the control with intense to moderate immunolabeling of the bronchiolar lining epithelium and surrounding mononuclear inflammatory cells. On the contrary, no significant differences were detected in the expression of the investigated apoptotic biomarkers between the control and the combined exposed group. We concluded that the exposure to either TCS or NaF resulted in significant perturbations in lung tissue after short term oral administration at variable instances but the co-exposure resulted in less severe toxicological consequences.