Ruan J.P., Chen J.D., Zeng J., Yang Z.G., Wang C.G., Hong Z. and Zuo Z.H.. 2019. Environmental Science and Pollution Research, 26(4): 3612-3620.

Oxidative stress is regarded as one of the most important factors associated with many diseases, such as atherosclerosis, cancer, and diabetes. Various chemicals are released into the environment, causing environmental pollution. Importantly, many of them may cause damage to organisms through oxidative stress. In this work, we investigated the possible protective effects of Nile tilapia (Oreochromis niloticus) scale collagen hydrolysate (TSCH) (molecular weight approximately 4 kDa) against tributyltin (TBT)-induced oxidative stress in vitro. The results showed that pretreatment with TSCH protected against decreases in cell viability and changes in cell morphology in HepG2 cells exposed to TBT. Treatment with TSCH reduced the TBT-induced elevation in malondialdehyde (MDA) levels in HepG2 cells in a dose-dependent manner. Pretreatment with TSCH increased glutathione reductase (GR) and superoxide dismutase (SOD) activity. Moreover, TSCH decreased the expression of the proapoptotic protein Bax, reducing apoptosis. These results suggest that the protective mechanism of TSCH may be associated with its ability to scavenge MDA, increase antioxidant enzyme activity and downregulate the expression of Bax.

Figure 1. Effect of TSCH on the morphology of HepG2 cells. a Non-treated culture. b Culture treated with 0.2 μM TBT. c Culture treated with 10 mg/mL TSCH + 0.2 μM TBT. d Culture treated with 20 mg/mL TSCH + 0.2 μM TBT. Representative images of HepG2 cells were observed by a Nikon TE 2000 inverted phase-contrast microscope (×20).

Figure 2. Effect of TSCH on the levels of Bcl-2 and Bax protein in HepG2 cells. The data are presented as mean ± SE (n = 5). Means of treatments not sharing a common letter are significantly different at P < 0.05 as assessed using one-way ANOVA followed by Duncan’s test.