Laboratory of Functional and Structural Biology, Institute of Biological Sciences, Federal University of Para, Street Augusto Correa N. 01, Guamá, Belém, Para, 66075-900, Brazil.
School of Dentistry, Federal University of Para, Belem, Para, Brazil.
Biol Trace Elem Res. 2018 Sep;185(1):135-142. doi: 10.1007/s12011-017-1230-9. Epub 2018 Jan 14.
Environmental and occupational mercury exposure is considered a major public health issue. Despite being well known that MeHg exposure causes adverse effects in several physiologic functions, MeHg effects on salivary glands still not completely elucidated. Here, we investigated the cellular MeHg-induced damage in the three major salivary glands (parotid, submandibular, and sublingual) of adult rats after chronic, systemic and low doses of MeHg exposure. Rats were exposed by 0.04 mg/kg/day over 60 days. After that, animals were euthanized and all three glands were collected. We evaluated total Hg accumulation, metallothionein I/II (MT I/II), α-smooth muscle actin (α-SMA), and cytokeratin 18 (CK18) immune expression. Our results have showed that MeHg is able to disrupt gland tissue and to induce a protective mechanism by MT I/II expression. We also showed that cell MT production is not enough to protect gland tissue against cellular structural damage seen by reducing marking of cytoskeletal proteins as CK18 and α-SMA. Our data suggest that chronic MeHg exposure in low-daily doses is able to induce cellular damage in rat salivary glands.
环境和职业性汞暴露被认为是一个主要的公共卫生问题。尽管众所周知，甲基汞（MeHg）暴露会对几种生理功能造成不良影响，但 MeHg 对唾液腺的影响仍未完全阐明。在这里，我们研究了慢性、系统性和低剂量 MeHg 暴露后成年大鼠的三种主要唾液腺（腮腺、颌下腺和舌下腺）中细胞 MeHg 诱导的损伤。大鼠每天暴露于 0.04mg/kg 持续 60 天。之后，处死动物并收集所有三个腺体。我们评估了总汞积累、金属硫蛋白 I/II（MT I/II）、α-平滑肌肌动蛋白（α-SMA）和细胞角蛋白 18（CK18）的免疫表达。我们的结果表明，MeHg 能够破坏腺体组织，并通过 MT I/II 的表达诱导一种保护机制。我们还表明，细胞 MT 的产生不足以保护腺体组织免受细胞结构损伤，如 CK18 和 α-SMA 标记减少。我们的数据表明，低日剂量的慢性 MeHg 暴露能够诱导大鼠唾液腺的细胞损伤。
