摘要:
低剂量中长期暴露下的氧化胁迫是砷对水生生物致毒的重要机制之一。本文通过对罗非鱼进行32 d的食物相砷暴露,测定不同时间点罗非鱼肝脏中谷胱甘肽(glutathione,GSH)含量和谷胱甘肽巯基转移酶(glutathione S-transferase,GST)活性,揭示不同价态无机砷对罗非鱼肝脏中GSH/GST的影响机制。经三价砷(As (Ⅲ))暴露后,砷含量在2 d内显著增加而在随后的30 d内无显著性差异;0~2 d内GSH含量显著增加,后降低,13 d后GSH含量均低于空白组;0~6 d GST活性均大于空白组,6~8 d GST活性降低,8 d后活性高于空白组,且32 d达到最大值。经五价砷(As (V))暴露后,罗非鱼肝脏中砷含量逐渐增加,在20 d时达到最大值而后无显著性差异;0~2 d时GSH含量降低,随后逐渐增加,在16 d达到最大值,16 d后GSH含量均低于空白组;0~8 d时GST被大量诱导合成,8~20 d时GST合成被抑制,20 d后活性增加,在32 d达到最大值。As (Ⅲ)和As (V)对罗非鱼GSH/GST的不同影响与其在罗非鱼体内的积累量有关。As (Ⅲ)暴露后各时间点罗非鱼肝脏中的砷含量与GSH含量呈统计学正相关,而As (V)暴露无明显相关性。这是因为As (V)进入罗非鱼肝脏后会还原为As (Ⅲ),进而GSH作为可提供巯基的还原剂而被大量消耗。另外,As (Ⅲ)暴露后各时间点罗非鱼肝脏中的砷含量与GST活性呈显著负相关,而As (V)暴露却呈现出很强的滞后性,这是由于进入生物体内的As (V)需转化为As (Ⅲ)后,才可直接作用于酶系统。可见,不同形态砷对水生生物的致毒机制需进一步深入研究。
Abstract:
Oxidative stress is crucial to understand the toxicity mechanism of aquatic species in arsenic mid-term exposure at low-dose. Based on the tilapia exposure to arsenic for 32 days, the content of glutathione (GSH) and the activity of glutathione S-transferase (GST) were measured at different time points during experimental period to address the oxidative stress mechanism of arsenic accumulation in liver. The study showed that after the As(Ⅲ) exposure the arsenic accumulation in liver was significantly increased in 2 days and no significant difference in the following 30 days; the content of GSH were significantly increased in 2 days and lower than that in the blank group after 13 days; at the same time GST activity were greater than that in the blank group in 2 days, then there was a fluctuation and reached the plateaus after 32 d exposure. After the As(V) exposure, the arsenic accumulation in liver was gradually increased and reached the plateaus after 20 days exposure, and GSH content decreased in 2 days and then gradually increased until to 16 d. GST activity increased significantly during the first 6-day exposure and decreased thereafter. The different effects of As(Ⅲ) and As(V) on tilapia GSH/GST are related to the accumulation of arsenic in tilapia. For As(Ⅲ), the accumulation of arsenic in liver positively correlated with the activity of GSH, while no significant correlation was observed between arsenic accumulation in liver and the content of GSH in As(V) exposure, which may be caused by the depletion of GSH as a reductant to provide sulfhydryl for arsenic biotransformation. For As(Ⅲ), the accumulation of arsenic in liver negatively correlated with the activity of GST. Similarly, the activity of GST for As(V) exposure negatively correlated with the lag of arsenic accumulation in liver. This can be explained by the transformation of As(V) to As(Ⅲ) before its complexation with GST in the liver of tilapia. The toxic mechanism of different forms of arsenic should be further studied to validate this assumption.
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