TY - JOUR
T1 - Protective Effects of Sodium Para-aminosalicylic Acid on Manganese-Induced Damage in Rat Pancreas
AU - Zhu, Xiaojuan
AU - Xie, Bingyan
AU - Liang, Dianyin
AU - Qin, Wenxia
AU - Zhao, Lin
AU - Deng, Yue
AU - Wen, Pingjing
AU - Xu, Fang
AU - Aschner, Michael
AU - Jiang, Yueming
AU - Ou, Shiyan
N1 - Funding Information:
Financial support was provided by grants from the National Natural Science Foundation of China (NSFC 81460505 and 81973094). MA was supported in part by grants from the National Institute of Environmental Health Sciences (NIEHS), R01ES10563 and R01ES07331.
Publisher Copyright:
© 2021, Springer Science+Business Media, LLC, part of Springer Nature.
PY - 2021/10
Y1 - 2021/10
N2 - Sodium p-aminosalicylic acid (PAS-Na) has been previously shown to protect the brain from manganese (Mn)-induced toxicity. However, the efficacy of PAS-Na in protecting other organs from Mn toxicity and the mechanisms associated with this protection have yet to be addressed. Therefore, here, we assessed pancreatic damage in response to Mn treatment and the efficacy of PAS-Na in limiting this effect, along with specific mechanisms that mediate PAS-Na’s protection. Mn exposure led to increased blood Mn content in dose- and time-dependent manner. Furthermore, subchronic Mn exposure (20 mg/kg for 8 weeks) led to pancreatic damage in a dose-dependent manner. In addition, the elevated Mn levels increased iron and decreased zinc and magnesium content in the pancreas. These effects were noted even 8 weeks after Mn exposure cessation. Mn exposure also affected the levels of amylase, lipase, and inflammatory factors such as tumor necrosis factor (TNF-α) and interleukin-1 β (IL-1β). PAS-Na significantly inhibited the increase in Mn concentration in both blood and pancreas, restored Mn-induced pancreatic damage, reversed the Mn-induced alterations in metal levels, and restored amylase and lipase concentrations. Taken together, we conclude that in rats, PAS-Na shows pharmacological efficacy in protecting the pancreas from Mn-induced damage.
AB - Sodium p-aminosalicylic acid (PAS-Na) has been previously shown to protect the brain from manganese (Mn)-induced toxicity. However, the efficacy of PAS-Na in protecting other organs from Mn toxicity and the mechanisms associated with this protection have yet to be addressed. Therefore, here, we assessed pancreatic damage in response to Mn treatment and the efficacy of PAS-Na in limiting this effect, along with specific mechanisms that mediate PAS-Na’s protection. Mn exposure led to increased blood Mn content in dose- and time-dependent manner. Furthermore, subchronic Mn exposure (20 mg/kg for 8 weeks) led to pancreatic damage in a dose-dependent manner. In addition, the elevated Mn levels increased iron and decreased zinc and magnesium content in the pancreas. These effects were noted even 8 weeks after Mn exposure cessation. Mn exposure also affected the levels of amylase, lipase, and inflammatory factors such as tumor necrosis factor (TNF-α) and interleukin-1 β (IL-1β). PAS-Na significantly inhibited the increase in Mn concentration in both blood and pancreas, restored Mn-induced pancreatic damage, reversed the Mn-induced alterations in metal levels, and restored amylase and lipase concentrations. Taken together, we conclude that in rats, PAS-Na shows pharmacological efficacy in protecting the pancreas from Mn-induced damage.
KW - Inflammatory factors
KW - Manganese
KW - Metal element
KW - Pancreas
KW - Sodium para-aminosalicylate
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U2 - 10.1007/s12011-020-02516-x
DO - 10.1007/s12011-020-02516-x
M3 - Article
C2 - 33405079
AN - SCOPUS:85099047145
SN - 0163-4984
VL - 199
SP - 3759
EP - 3771
JO - Biological Trace Element Research
JF - Biological Trace Element Research
IS - 10
ER -
