Atrazine is a synthetic triazine herbicide widely used in agriculture, particularly in the cultivation of corn, sugarcane, and sorghum, to control weeds. Plants rely on photosynthesis, the process of converting light energy into chemical energy, for survival and growth. The herbicidal action of atrazine specifically targets the molecular machinery responsible for this energy conversion, disrupting the plant’s energy production pathway.
The Photosynthesis Process Targeted by Atrazine
Photosynthesis begins with the light-dependent reactions, which occur within the thylakoid membranes of the plant’s chloroplasts. These reactions capture solar energy and involve a protein complex called Photosystem II (PSII), which acts as the starting point for the electron transport chain.
PSII absorbs light, exciting electrons that are replaced by splitting a water molecule, releasing oxygen. These high-energy electrons are passed along acceptor molecules embedded in the thylakoid membrane. This electron flow generates the energy carriers, adenosine triphosphate (ATP) and nicotinamide adenine dinucleotide phosphate (NADPH), which power the subsequent stages of sugar production.
Blocking the Electron Transport Chain
Atrazine is classified as a Photosystem II inhibitor and acts as a competitive inhibitor within the PSII complex. The herbicide targets a site on the D1 reaction center protein, a core component of Photosystem II. This D1 protein normally binds the plastoquinone (Q\(_B\)) molecule, which accepts and shuttles electrons away from PSII.
When atrazine enters the chloroplast, it binds to the D1 protein site, displacing plastoquinone. The binding of atrazine physically plugs this site, preventing the transfer of electrons out of Photosystem II and into the electron transport chain. This blockage halts the entire chain.
The cessation of electron transport means the plant cannot complete the light-dependent reactions. This prevents the formation of the energy carriers, ATP and NADPH. These molecules are indispensable for the Calvin cycle, where carbon dioxide is fixed into sugars for plant metabolism and growth.
The Immediate Consequences for Plant Health
The blocked electron flow results in the plant’s inability to synthesize the energy molecules needed for growth and survival. Without ATP and NADPH production, the plant starves because it cannot convert carbon dioxide into sugars, leading to plant death.
The blockage also creates a damaging situation within the Photosystem II complex. Since electrons cannot be passed on, the absorbed energy becomes trapped within the system. This excess energy leads to the formation of Reactive Oxygen Species (ROS) or free radicals.
The accumulation of ROS creates severe oxidative stress within the plant cells. This stress damages cellular components, including the degradation of the D1 protein, the destruction of chlorophyll pigments, and the breakdown of cell membranes. This cellular necrosis causes the visible symptoms of wilting, chlorosis (yellowing), and tissue death that characterize the herbicidal effect.
Atrazine’s Role as a Selective Herbicide
Atrazine’s value stems from its selective toxicity, meaning it kills weeds without harming the crop. This selectivity is not due to a difference in the target site, as the D1 protein in crops and weeds is nearly identical. The difference lies in the plant’s ability to detoxify the atrazine molecule before it can reach the chloroplast.
Tolerant crops, such as corn and sugarcane, possess metabolic defense systems. These crops express high levels of detoxification enzymes, notably glutathione S-transferases (GSTs). GSTs rapidly catalyze a chemical reaction that binds atrazine to a protective compound called glutathione.
This conjugation process converts the phytotoxic atrazine into a water-soluble, non-phytotoxic derivative. This neutralized form is stored in the plant’s vacuole or expelled from the cell, preventing it from binding the D1 protein. Susceptible broadleaf weeds, however, lack this efficient enzymatic defense mechanism, allowing the atrazine to rapidly accumulate in the chloroplasts and halt photosynthesis.