식품안전 ≫ 잔류농약, 환경물질

잔류농약 : 제초제 작용기작

잔류 농약
- 과일 껍질의 잔류농약 : 안전한 수준
- 농약 : 소비자 의식 변화 기대
- 농약과 안전성
- 제초제 : 작용기작
- 제초제의 독성 및 환경에 영향
- 제초제 : 글리포세이트
- 제초제 : 그라목손

2007년 5월 현재 국내 제초제는 총 297개 품목, 418개 상표이다.
세계적으로 사용되고 있는 제초제 유효성분이 300종 이하이고, 국내는 101종으로서
작용기작에 따라 구분하면, 생장조절 저해제 8종, 유묘생장 저해제 31종, 광합성 저해제 10종, 아미노산합성 저해제 23종, 지질합성 저해제 9종, 색소체 저해제 6종, 세포막 저해제 9종, 작용기작 미확인 제초제 5종으로 되어있다.

List of mechanisms found in modern herbicides
- ACCase inhibitors : 지방합성 방해 Acetyl coenzyme A carboxylase (ACCase) is part of the first step of lipid synthesis. Thus, ACCase inhibitors affect cell membrane production in the meristems of the grass plant. The ACCases of grasses are sensitive to these herbicides, whereas the ACCases of dicot plants are not.

- ALS inhibitors: 분지형 아미노산 합성방해 the acetolactate synthase (ALS) enzyme is the first step in the synthesis of the branched-chain amino acids (valine, leucine, and isoleucine). These herbicides slowly starve affected plants of these amino acids, which eventually leads to inhibition of DNA synthesis. They affect grasses and dicots alike. The ALS inhibitor family includes various sulfonylureas (SUs) (such as Flazasulfuron and Metsulfuron-methyl), imidazolinones (IMIs), triazolopyrimidines (TPs), pyrimidinyl oxybenzoates (POBs), and sulfonylamino carbonyl triazolinones (SCTs). The ALS biological pathway exists only in plants and not animals, thus making the ALS-inhibitors among the safest herbicides.[6]

- EPSPS inhibitors: 방향족 아미노산 합성방해 Enolpyruvylshikimate 3-phosphate synthase enzyme (EPSPS) is used in the synthesis of the amino acids tryptophan, phenylalanine and tyrosine. They affect grasses and dicots alike. Glyphosate (Roundup) is a systemic EPSPS inhibitor inactivated by soil contact.

- Synthetic auxins : 성장 교란 Synthetic auxins mimic this plant hormone. They have several points of action on the cell membrane, and are effective in the control of dicot plants. 2,4-D is a synthetic auxin herbicide.

- Photosystem II inhibitors reduce electron flow from water to NADP+ at the photochemical step in photosynthesis. They bind to the Qb site on the D1 protein, and prevent quinone from binding to this site. Therefore, this group of compounds causes electrons to accumulate on chlorophyll molecules. As a consequence, oxidation reactions in excess of those normally tolerated by the cell occur, and the plant dies. The triazine herbicides (including atrazine) and urea derivatives (diuron) are photosystem II inhibitors.[7]

- Photosystem I inhibitors steal electrons from the normal pathway through FeS to Fdx to NADP+ leading to direct discharge of electrons on oxygen. As a result, reactive oxygen species are produced and oxidation reactions in excess of those normally tolerated by the cell occur, leading to plant death. Bipyridinium herbicides (such as diquat and paraquat) inhibit the FeS to Fdx step of that chain, while diphenyl ether herbicides (such as nitrofen, nitrofluorfen, and acifluorfen) inhibit the Fdx to NADP+ step.[7]

- HPPD inhibitors : 카로틴 합성 억제 inhibit 4-Hydroxyphenylpyruvate dioxygenase, which are involved in tyrosine breakdown.[8] Tyrosine breakdown products are used by plants to make carotenoids, which protect chlorophyll in plants from being destroyed by sunlight. If this happens, the plants turn white due to complete loss of chlorophyll, and the plants die.[9][10] Mesotrione and sulcotrione are herbicides in this class; a drug, nitisinone, was discovered in the course of developing this class of herbicides.