Of four types of dietary fat (monounsaturated, polyunsaturated, saturated and trans), focus recently has been on trans fat. Abundant in margarine, shortening, packaged baked goods and French fries to name a few, trans fat is a widely used ingredient for food manufacturers because it is cheap and contributes to increased shelf life. It is listed as "partially hydrogenated vegetable oil" and "vegetable shortening" on product ingredient lists.

Hydrogenation is process of heating an oil and passing hydrogen bubbles through it. The fat's density is increased, and food manufacturers use it frequently because it gives products a richer butter flavor. Saturated butter is much more expensive to use, so manufacturers reduce costs by using partially hydrogenated oils.

Partially hydrogenated oils, however, have a much different effect on body than even demonized saturated fats. We all know that we need to limit saturated fat in our diets, but specific amounts, although small, have been deemed acceptable, and even help to facilitate a variety of processes for body. Trans fat, however, provides no positive effects whatsoever.

Studies have consistently shown that trans fat raises LDL (bad) cholesterol and lowers HDL (good) cholesterol. It contributes to clogging of arteries and type 2 diabetes. Trans fat has also been linked to an estimated 30,000 or more premature heart disease deaths each year.

In March 2004, Food and Drug Administration updated their website pages concerning trans fat and regulations concerning labeling laws. Although FDA first proposed trans fat labeling in 1999, it wasn't until July 2003 that Health and Human Services Secretary Tommy Thompson announced new trans fat ruling. Even then, guidelines proved to be less than acceptable to health experts who were pushing for immediate regulations: ruling gave manufacturers until January 1, 2006 to comply.

Cancer cells and normal cells are known to respond differently to nutrients and drugs that affect glutathione status.

Numerous studies have shown that tumor cells have elevated levels of glutathione levels, which confers resistance to chemotherapy drugs.

One of challenges of cancer therapy is how to deplete tumor cells of glutathione, so as to make them more vulnerable to effects of chemotherapy drugs, while at same time allowing normal cells to remain relatively unaffected by chemotherapeutic drugs.

A number of new findings have emerged that take into consideration role of glutathione in pathways that promote programmed cell death (apoptosis) in cancer cells.

A German study has reported that glutathione (GSH) plays a critical role in cellular mechanisms that result in cell death. The study found that cancer cells resistant to apoptosis had higher intracellular GSH levels.

Depletion of glutathione in these tumor cells made them more vulnerable to effects of anticancer drugs or gene that promotes apoptosis (CD95 or APO-1/Fas). The researchers concluded that apoptosis resistance in tumor cells depends, at least in part, on intracellular GSH levels. (1)

In another study conducted in Spain, researchers found that lowering GSH concentration may be convenient not only for efficiency of chemotherapy, but also to induce a rather fast and direct apoptosis mechanism in tumor cells. (2)

Based on that premise that glutathione-S-transferase enzyme is expressed at high levels in many tumors, researchers at Fox Chase Cancer Center in Pennsylvania, went on to design a novel prodrug (PABA/NO).

The glutathione-s-transferase in tumor cells converts PABA/NO to lethal nitric oxide, resulting in death of tumor cell. The prodrug was shown to have antitumor effects in an animal model for human ovarian cancer. (3)