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首页> 外文期刊>Life sciences >Effects of ascorbic acid on lead induced alterations of synaptic transmission and contractile features in murine dorsiflexor muscle.
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Effects of ascorbic acid on lead induced alterations of synaptic transmission and contractile features in murine dorsiflexor muscle.

机译：抗坏血酸对铅诱导的小鼠背屈肌突触传递和收缩功能改变的影响。

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Lead is a common environmental toxin that affects neuromuscular junction and potentially might cause muscle weakness. Antioxidants like ascorbic acid may protect against lead induced myopathy. The present study measured isometric twitch tensions (evoked either directly by muscle stimulation or indirectly by nerve stimulation) to study effects of ascorbic acid on lead induced alterations at murine dorsiflexor skeletal muscle. Resting membrane potentials (RMPs), endplate potentials (EPPs) and miniature endplate potentials (MEPPs) were also recorded. Forty animals were divided into four groups of n = 10 each. (10 control, 10 lead alone, 10 ascorbic acid alone, 10 lead treated plus ascorbic acid). Lead (1 mg/kg) i.p, was administered daily for 2 weeks before the recording day and ascorbic acid (200 mg/kg, i.p) was given daily for 3 weeks prior to the experiment day. Lead treatment reduced twitch tension significantly (from 4.3 +/- 0.5 g to 2.7 +/- 0.2 g) and delayed half time of decay compared to the control. Similarly MEPPs frequencies were reduced following lead treatment. Application of ascorbic acid prevented twitch tension reduction in lead treated mice (3.3 +/- 0.3 g) and reversed lead induced delay in half time of decay. The negative actions of lead treatment on MEPPs frequencies were also modified with ascorbic acid. It appears that ascorbic acid exerts a protective role against lead induced peripheral nerve and muscle dysfunction. This effect of ascorbic acid on lead induced neuromyopathy is probably mediated via a free radical scavenging mechanism or modification of Ca(2+) homeostasis.
机译：铅是一种常见的环境毒素，会影响神经肌肉连接，并可能导致肌肉无力。像抗坏血酸这样的抗氧化剂可以预防铅引起的肌病。本研究测量了等距抽搐张力（通过肌肉刺激直接引起或通过神经刺激间接引起）来研究抗坏血酸对铅引起的鼠背屈骨骼肌改变的影响。还记录了静息膜电位（RMP），终板电位（EPP）和微型终板电位（MEPP）。将40只动物分成n ＝ 10的四组。 （10个对照，10个铅单独，10个抗坏血酸单独，10个铅加抗坏血酸处理）。在记录日之前的2周内每天i.p给予铅（1 mg / kg），在实验日之前的3周内每天给予抗坏血酸（200 mg / kg，i.p）。与对照相比，铅处理可显着降低抽搐张力（从4.3 +/- 0.5 g降低至2.7 +/- 0.2 g），并延迟半衰期。同样，铅处理后MEPPs频率降低。抗坏血酸的应用防止了铅处理的小鼠（3.3 +/- 0.3 g）的抽搐张力降低，并且扭转了铅诱导的半衰期延迟。铅处理对MEPPs频率的负面作用也被抗坏血酸修饰。似乎抗坏血酸对铅引起的周围神经和肌肉功能障碍具有保护作用。抗坏血酸对铅诱导的神经肌病的影响可能是通过自由基清除机制或Ca（2+）稳态的修饰介导的。

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