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The article provides information on a study that examines lycopene effects on rat normal prostate and prostate tumor tissue. Epidemiological evidence links tomato consumption with reduced risk of prostate cancer. Prostate cancer remains a severe health problem throughout the Western world, and the success in treating advanced prostate cancer remains poor. Therefore, the importance of prevention through dietary measures is growing. Lycopene, a non-provitamin A carotenoid and the red pigment of tomatoes, is considered the major active compound in tomatoes. The health function of lycopene has been mainly linked to its potent antioxidant effects resulting in protection against oxidative DNA damage in vitro and in vivo. Lycopene also inhibits cell proliferation, at least in part due to its interference with insulin-like growth factor-I. In this study, to obtain insight into the in vivo mechanisms by which lycopene and/or vitamin E contribute to prostate cancer risk reduction, researchers used the MatLyLu Dunning prostate cancer model. In this model, thirty male Copenhagen rats were randomly assigned to 5 groups. The 2 control groups were non-supplemented controls and placebo-supplemented controls.

Focuses on a study which investigated the effect of lycopene on gene regulation in normal rat prostate. Uptake of lycopene in prostate tissue; Noninterference of lycopene with normal prostate growth; Activity of lycopene in normal prostate.

Renal cell carcinoma (RCC) is the most frequent upper urinary tract cancer in humans and accounts for 80–85% of malignant renal tumors. Eker rat represents a unique animal model to study RCC since these rats develop spontaneous renal tumors and leiomyoma, which may be due to tuberous sclerosis 2 (TSC2) mutation resulting in the activation of the mammalian target of rapamycin (mTOR) pathway. This study examines the role of a lycopene-rich diet in the development of RCC in the TSC2 mutant Eker rat model. Ten-week old female Eker rats ( n = 90) were assigned in equal numbers to receive 0, 100 or 200 mg/kg of lycopene as part of their daily diet. After 18 months the rats were sacrificed and the kidneys were removed. Immunohistochemical staining with antibodies against mTOR, phospho-S6 and EGFR were performed, as well as hematoxylin–eosin staining for histologic examination of the tumors. Tumors were counted and measured in individual kidneys. Presence of tumor decreased from 94% in control animals to 65% in the experimental group, but the difference was not statistically significant ( P < 0.12). However, mean numbers of renal carcinomas were statistically significantly decreased in the lycopene-treated rats ( P < 0.008) when compared to untreated controls. In the lycopene group, tumor numbers decreased ( P < 0.002) and the numbers tended to decrease linearly ( P < 0.003) as supplemental lycopene increased from 0 to 200. Control rats fed only basal diet had a greater length of tumors (23.98 mm) than rats fed lycopene supplement groups (12.90 mm and 11.07 mm) ( P < 0.05). Moreover tumor length decreased ( P < 0.02) and tumor length tended to decrease linearly ( P < 0.03) as supplemental lycopene increased from 0 to 200 mg/kg. All tumors showed strong staining with antibodies against mTOR, phospho-S6 and EGFR. In conclusion, dietary supplementation with lycopene attenuates the development of renal cell cancers in the predisposed TSC2 mutant Eker rat model. These results suggest that lycopene may play a role in the prevention of RCC. [ABSTRACT FROM AUTHOR]

Abstract: Oxidative stress and mitochondrial dysfunction are known to play important roles in type 2 diabetes mellitus (T2DM) and insulin resistance. However, the pathology of T2DM remains complicated; in particular, the mechanisms of mitochondrial dysfunction in skeletal muscle and other insulin-sensitive tissues are as yet unclear. In the present study, we investigated the underlying mechanisms of oxidative stress and mitochondrial dysfunction by focusing on mitochondrial dynamics, including mitochondrial biogenesis and autophagy, in skeletal muscle of a nonobese diabetic animal model — the Goto–Kakizaki (GK) rat. The results showed that GK rats exhibited impaired glucose metabolism, increased oxidative stress and decreased mitochondrial function. These dysfunctions were found to be associated with induction of LC3B, Beclin1 and DRP1 (key molecules mediating the autophagy pathway), while they appeared not to affect the mitochondrial biogenesis pathway. In addition, (−)-epigallocatechin-3-gallate (EGCG) was tested as a potential autophagy-targeting nutrient, and we found that EGCG treatment improved glucose tolerance and glucose homeostasis in GK rats, and reduced oxidative stress and mitochondrial dysfunction in skeletal muscle. Amelioration of excessive muscle autophagy in GK rats through the down-regulation of the ROS-ERK/JNK-p53 pathway leads to improvement of glucose metabolism, reduction of oxidative stress and inhibition of mitochondrial loss and dysfunction. These results suggest (a) that hyperglycemia-associated oxidative stress may induce autophagy through up-regulation of the ROS-ERK/JNK-p53 pathway, which may contribute to mitochondrial loss in soleus muscle of diabetic GK rats, and (b) that EGCG may be a potential autophagy regulator useful in treatment of insulin resistance. [Copyright &y& Elsevier]