Torularhodin is one of the principal carotenoids in Sporidiobolus pararoseus and has a similar structure to that of lycopene. The present work was to elucidate its anti-cancer activity on androgen-dependent prostate cancer LNCaP cells and androgen-independent PC-3 cells using lycopene as a control. WST-1 assay showed that the efficiency of torularhodin was much better than lycopene on both prostate cell lines. Flow cytometry results demonstrated that its apoptotic induction was associated with loss of mitochondrial membrane potential and increased intracellular calcium concentration. Quantitative real-time polymerase chain reaction and western blot data revealed that torularhodin changed the expression ratio of pro-apoptotic to anti-apoptotic Bcl-2 family members. Moreover, we found that torularhodin significantly down-regulated the expression levels of androgen receptor (AR) and prostate-specific antigen (PSA) expression in LNCaP cells. The present results indicate that torularhodin inhibited the growth of LNCaP and PC-3 cells via the mitochondria-mediated pathway and the down-regulation of AR expression.

Diabetic nephropathy (DN) is the major life-threatening complication of diabetes, and oxidative stress takes part in its initiation and development. This study was performed to evaluate the effects of carotenoids from Sporidiobolus pararoseus (CSP) on the renal function and oxidative stress status of mice with streptozotocin (STZ)-induced DN. The results indicated that CSP significantly attenuated symptoms of STZ-induced DN shown by decreased fasting blood glucose, reduced urine volume, urine albumin, serum creatinine and serum urea nitrogen, and improved kidney histological morphology. Furthermore, biochemical analysis of serum and kidney revealed a marked increase in oxidative stress of DN mice as evidenced by reduced total antioxidant capacity (T-AOC), decreased activity of antioxidant enzyme -superoxide dismutase (SOD) and increased level of malondialdehyde (MDA). However, treatment with CSP improved oxidative stress status in DN mice as compared with the mice in model group. Exploration of the potential mechanism validated that CSP ameliorated the oxidative stress status in DN mice by activating the expressions of Nrf2, NQO-1, HO-1, GST and CAT in kidney. These data revealed that CSP may retard the progression of DN by ameliorating renal function, improving the oxidative stress status and activating the Nrf2/ARE pathway.