The primary metabolic characteristic of malignant cells is an increased uptake of glucose and its anaerobic metabolism. We studied the expression and function of the glucose transporters in human breast cancer cell lines and analyzed their expression in normal and neoplastic primary human breast tissue. Hexose uptake assays and immunoblotting experiments revealed that the breast carcinoma cell lines MCF-7 and MDA-468 express the glucose transporters GLUT1 and GLUT2, isoforms expressed in both normal and neoplastic breast tissue. We also found that the breast cancer cell lines transport fructose and express the fructose transporter GLUT5. Immunolocalization studies revealed that GLUT5 is highly expressed in vivo in human breast cancer but is absent in normal human breast tissue. These findings indicate that human breast cancer cells have a specialized capacity to transport fructose, a metabolic substrate believed to be used by few human tissues. Identification of a high-affinity fructose transporter on human breast cancer cells opens opportunities to develop novel strategies for early diagnosis and treatment of breast cancer.

Social isolation in rodents is the most well characterized animal model for early stressful experiences and their neurobehavioral consequences. The present study analyzed the effects of early social isolation on the expression of the calcium binding protein calbindin-D28k (CAD) and dendritic arborization in the medial prefrontal cortex (mPFC) of the rat. Sprague-Dawley male rats were reared either under isolation or social conditions from 21 to 51 postnatal days. At the end of this period the animals were behaviorally evaluated in the open-field test, sacrificed, and mPFC serial sections were processed either for immunocytochemical labeling against CAD or Golgi-Cox-Sholl staining. Isolated-reared rats exhibited a dramatic decrease in the number of CAD immunoreactive neurons and a significant dendritic atrophy of layer II/III pyramidal cells in association with a reduced exploratory behavior.

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Diethylstilbestrol (DES), a transplacental endocrine-disrupting chemical, was prescribed to pregnant women for several decades. The number of women who took DES is hard to know precisely, but it has been estimated that over 10 million people have been exposed around the world. DES was classified in the year 2000 as carcinogenic to humans. The deleterious effects induced by DES are very extensive, such as abnormalities or cancers of the genital tract and breast, neurodevelopmental alterations, problems associated with socio-sexual behavior, and immune, pancreatic and cardiovascular disorders. Not only pregnant women but also their children and grandchildren have been affected. Epigenetic alterations have been detected, and intergenerational effects have been observed. More cohort follow-up studies are needed to establish if DES effects are transgenerational. Even though DES is not currently in use, its effects are still present, and families previously exposed and their later generations deserve the continuity of the research studies.

It has been demonstrated that postweaning social isolation alters dendritic development in the medial prefrontal cortex (mPFC) of the rat. In addition, (–)-deprenyl, a monoamine oxidase B (MAO-B) inhibitor, promotes dendritic growth in prefrontocortical pyramidal cells. This study examined whether prefrontocortical dendritic developmental impairment induced by postweaning social isolation is attenuated by chronic (–)-deprenyl administration. Weanling Sprague-Dawley male rats were randomly reared in social and isolated environments between postnatal days 21 and 51 (P21–P51). At P52, half of the animals were behaviorally evaluated in the open-field test and sacrificed for histological analysis. The remaining isolated rats were subdivided into saline- and daily (–)-deprenyl-treated animals for 30 additional days (P52–P82). Socially-reared rats remained undisturbed except for daily saline administration. At P82, all animals were behaviorally evaluated and sacrificed for histological analysis. Dendritic quantification of the Golgi-Cox-Sholl-stained neurons indicated that chronic (–)-deprenyl administration partially compensated the dendritic growth impairment induced by social isolation. In addition, both isolated-saline- and (–)-deprenyl-treated rats showed a sustained locomotor hyperactivity in the open-field test.