我可以說我是專業研究百草枯的麽？我985高校導師和我的方案可能可以治療百草枯中毒，雖然我們不知道有誰會用我們的方案來治。
本人有機化學博士畢業，目前在某省屬一本高校工作，拿過一次國家自然科學基金，研究百草枯的超分子化學已經八年了。。。。
百草枯的毒性主要來自於抑制生物體的氧化態磷酸輔酶NAD(NADP)～還原態磷酸輔酶NADH(NADPH)的氧化還原迴圈過程。百草枯會切斷這個過程，所有依賴於磷酸輔酶的生物過程都會因此中斷，這是百草枯的毒性機制。具體的是百草枯可以氧化還原態磷酸輔酶，使磷酸輔酶全部變成氧化態失去能量傳輸功能。百草枯的直接毒性並不強，不像敵敵畏之類的有機磷農藥，直接產生呼吸神經中樞抑制、心臟功能抑制之類的效果，所以會有幾天的存活期。比較形象的比喻是，假如ATP是人體的現金，磷酸輔酶就相當於人體的銀行帳戶支付寶，百草枯會把人體的銀行帳戶支付寶全部銷戶，一旦現金用完了，就餓死了。
百草枯的棘手的地方是太強的水溶性，樓上有人說有脂溶性是錯的，只有水溶性，沒有脂溶性，而且水溶性強的和食鹽一樣，並且分子很小可以穿透細胞膜，所以全身所有的細胞都會受影響。從這個角度看，百草枯無救是因為進入人體就會全身分散，難以清除。有機磷農藥能救是因為吸收慢，局部聚集，洗胃很管用。百草枯喝了，就像喝了鹽水一樣，很快被血液吸收。
我的導師09年發表了一篇【journal of medicinal chemsitry】，轉譯過來是【美國藥物化學】，題目是Highly Effective Binding of Viologens by p-Sulfonatocalixarenes for the Treatment of Viologen Poisoning，磺化杯芳烴對紫精類的高效鍵合並用於紫精中毒的解毒。紫精是我們的叫法，常見的包括百草枯和敵草快兩種。原理上，我們的辦法是用一個分子結合百草枯，讓百草枯失去對還原態磷酸輔酶的氧化性，有興趣的可以找找這篇論文看看
該論文一作不是我，我做了結構類似的原創分子
貼一段上來
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
