Mechanism of metolachlor action due to alterations in cell cycle progression.

Metolachlor, a commonly used herbicide in the Midwestern USA, functions by inhibiting chlorophyll and protein synthesis in target plants. Herbicide exposure has led to detrimental effects in several organisms, affecting their growth and behavior; however, its mechanism of action in nontarget organisms is not yet clear. The EPA does not currently have enforceable regulations for maximal limits allowed in drinking water.

Cellular effects of metolachlor exposure on human liver (HepG2) cells.

Metolachlor is one of the most commonly used herbicides in the United States. Protein synthesis is inhibited when roots and shoots of susceptible plants absorb this synthetic herbicide. While quite effective in killing weeds, several studies have shown that exposure to metolachlor results in decreased cell proliferation, growth and reproductive ability of non-target organisms.

Atrazine exposure leads to altered growth of HepG2 cells.

Atrazine is one of the most commonly used herbicides in the United States. While effective on target plants, it has been associated with harmful health effects in non-target organisms such as fish, amphibians and mammals. In this study, growth effects on human liver cells were determined after exposure to increasing concentrations of this herbicide.

Low-level atrazine exposure decreases cell proliferation in human fibroblasts.

There is continuing concern that release of certain chemicals into the environment leads to human exposure to toxins, particularly through contaminated ground and surface waters. The triazine herbicide atrazine (2-chloro-4-ethylamine-6-isopropylamino-S-triazine) is routinely found as a contaminant in many surface and groundwaters. Little is known of the long-term effects of atrazine exposure on human cells.