The Protective Role of Hyaluronic Acid in Cr(VI)-Induced Oxidative Damage in Corneal Epithelial Cells.

Wei Wu,Tao Li,Yu Wang,Lingfang Feng,Hua Jiang,Jianlin Lou,Hailing Xia,Shibo Ying,Riping Chen,Xinnian Guo,Yixiao Zhang,Tianhui Chen

doi:10.1155/2017/3678586

Abstract

Cr(VI) exposure could produce kinds of intermediates and reactive oxygen species, both of which were related to DNA damage. Hyaluronan (HA) has impressive biological functions and was reported to protect corneal epithelial cells against oxidative damage induced by ultraviolet B, benzalkonium chloride, and sodium lauryl sulfate. So the aim of our study was to investigate HA protection on human corneal epithelial (HCE) cells against Cr(VI)-induced toxic effects. The HCE cell lines were exposed to different concentrations of K2Cr2O7 (1.875, 3.75, 7.5, 15.0, and 30 μM) or a combination of K2Cr2O7 and 0.2% HA and incubated with different times (15 min, 30 min, and 60 min). Our data showed that Cr(VI) exposure could cause decreased cell viability, increased DNA damage, and ROS generation to the HCE cell lines. But incubation of HA increased HCE cell survival rates and decreased DNA damage and ROS generation induced by Cr(VI) in a dose- and time-dependent manner. We report for the first time that HA can protect HCE cells against the toxicity of Cr(VI), indicating that it will be a promising therapeutic agent to corneal injuries caused by Cr(VI).

Highlights

Chromium (Cr) exists in many states, and the forms of hexavalent chromium [Cr(VI)] and trivalent chromium [Cr(III)] are found commonly in the environment
The balance between oxidants and antioxidants may be broken by overproduced reactive oxygen species (ROS), which can cause oxidative stress such as lipid peroxidation (LPO), decreased cell viability, increased DNA damage, and apoptosis [13]
It was reported that high-molecular weight hyaluronan (HMWHA, 1000 kDa) could protect corneal epithelial cells against oxidative damage induced by ultraviolet B [24, 25], benzalkonium chloride [22], sodium lauryl sulfate [26], and so on

Summary

Introduction

Chromium (Cr) exists in many states, and the forms of hexavalent chromium [Cr(VI)] and trivalent chromium [Cr(III)] are found commonly in the environment. It is widely accepted that cellular reduction of Cr(VI) is an activation process that generates variable intermediates [Cr(V) and Cr(IV)] and reactive oxygen species (ROS) [8,9,10,11]. The balance between oxidants and antioxidants may be broken by overproduced ROS, which can cause oxidative stress such as lipid peroxidation (LPO), decreased cell viability, increased DNA damage, and apoptosis [13]. Oxidative stress can play a major role in inducing genetic and epigenetic alterations to organisms and is associated with carcinogenesis [8, 9, 14,15,16] Both in vivo and in vitro studies have reported that Cr(VI) exposure could induce oxidative stress, which is one of the mechanisms of toxicity of Cr(VI). There are very limited data reporting the toxic effects and mechanisms of Cr(VI) on the eye

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