我可以说我是专业研究百草枯的么？我985高校导师和我的方案可能可以治疗百草枯中毒，虽然我们不知道有谁会用我们的方案来治。
本人有机化学博士毕业，目前在某省属一本高校工作，拿过一次国家自然科学基金，研究百草枯的超分子化学已经八年了。。。。
百草枯的毒性主要来自于抑制生物体的氧化态磷酸辅酶NAD(NADP)～还原态磷酸辅酶NADH(NADPH)的氧化还原循环过程。百草枯会切断这个过程，所有依赖于磷酸辅酶的生物过程都会因此中断，这是百草枯的毒性机制。具体的是百草枯可以氧化还原态磷酸辅酶，使磷酸辅酶全部变成氧化态失去能量传输功能。百草枯的直接毒性并不强，不像敌敌畏之类的有机磷农药，直接产生呼吸神经中枢抑制、心脏功能抑制之类的效果，所以会有几天的存活期。比较形象的比喻是，假如ATP是人体的现金，磷酸辅酶就相当于人体的银行账户支付宝，百草枯会把人体的银行账户支付宝全部销户，一旦现金用完了，就饿死了。
百草枯的棘手的地方是太强的水溶性，楼上有人说有脂溶性是错的，只有水溶性，没有脂溶性，而且水溶性强的和食盐一样，并且分子很小可以穿透细胞膜，所以全身所有的细胞都会受影响。从这个角度看，百草枯无救是因为进入人体就会全身分散，难以清除。有机磷农药能救是因为吸收慢，局部聚集，洗胃很管用。百草枯喝了，就像喝了盐水一样，很快被血液吸收。
我的导师09年发表了一篇【journal of medicinal chemsitry】，翻译过来是【美国药物化学】，题目是Highly Effective Binding of Viologens by p-Sulfonatocalixarenes for the Treatment of Viologen Poisoning，磺化杯芳烃对紫精类的高效键合并用于紫精中毒的解毒。紫精是我们的叫法，常见的包括百草枯和敌草快两种。原理上，我们的办法是用一个分子结合百草枯，让百草枯失去对还原态磷酸辅酶的氧化性，有兴趣的可以找找这篇论文看看
该论文一作不是我，我做了结构类似的原创分子
贴一段上来
Introduction
Viologens are one class of significant redox couples,1 widely utilized not only as herbicides2 but also as probes to study
DNA and zeolites,3 as components of electrochromic display devices,4 and as prooxidants in stress tests.5-7 Two typical
species of viologens, paraquat (PQ
) and diquat (DQ), are effective, nonselective, and quick acting herbicides8 that are used by millions of growers and more than 100 crops in over 120 countries all over the world. Moreover, they are also
acutely toxic agrochemicals, and their high toxicity has long posed formidable risks to human health,9 society, and the environment. Absorption of viologens into the digestive tract, respiratory t
First, we employed 40 mice, which were divided into four groups stochastically. The first control group was administered with normal saline (0.9% w/v NaCl; 100 μL/20 g of body weight). The second group was administered with a solution of C5AS alone (9.7% w/v C5AS; 100 μL/20 g of body weight). The third group was administered with a solution of PQ2þ (2.4% w/v PQ2þ; 100 μL/20 g of body weight) according to the published LD50 value in mice (120 mg/kg of body weight; per os).45 The fourth group was administered with a solution of the C5AS 3 PQ2þ complex
(12.1% w/v C5AS 3 PQ2þ complex; 100 μL/20 g of body weight). We watched these experimental mice for 13 days
following the administrations and obtained the mortality rate for each group (Figure 7a). On day 14, the living mice were then sacrificed for weighing (see Figure S1a, Supporting Information), followed by sampling the liver and lung tissues
for pathological examination. All mice in group 2 remained alive for the duration of the experiment, and the average
weight of group 2 (33.4 ( 2.9 g) was statistically equivalent to that of group 1 (32.8 ( 3.8 g) (P > 0.05), which indicates that C5AS is innocuous to the mice in accordance with the previously published results for p-sulfonatocalix[n]arenes.33
Recently, the first in vivo studies of the biodistribution and pharmacokinetics of C4AS with regard to mice by the method of radioisotopic labeling have been described by Coleman et al.,46 which also shows that there is no acute toxicity for doses up to 100 mg/kg and the molecule is rapidly
cleared via elimination in urine. There is no significant uptake in the organs, and particularly in the liver and spleen.
The mortality rate of group 3 was 90%, and the weight of the surviving mouse was only 14.0 g, which clearly demonstrates
the serious toxicity of PQ2þ to the mice. The mortality rate of group 4 was decreased to 20%. Moreover, in stark contrast to group 3, the average weight of group 4 (30.8 ( 5.7 g) was statistically equivalent to those of groups 1 and 2 (P > 0.05). All of these data indicate that the complexation of C5AS can markedly inhibit the fatal toxicity of PQ2þ. The gross changes of lung and liver were observed by the naked eye (see Figure S1b and S2, Supporting Information). The tissues
were fixed and ped for microscopic examination of the structure (Figure 7b,c). No appreciable pathological changes
were observed in the lungs and livers of mice belonging not only to groups 1 and 2, but also those in group 4. In contrast,
the microscopic examination of lungs and livers of the surviving mouse in group 3 showed a massive destruction
of structures of the tissues. To further investigate the
