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(-)-Hydroxycitric acid (HCA), a natural extract from the dried fruit rind of Garcinia cambogia (family Guttiferae), is a popular supplement for weight management. The dried fruit rind has been used for centuries as a condiment in Southeastern Asia to make food more filling and satisfying. A significant number of studies highlight the efficacy of Super CitriMax (HCA-SX, a novel 60% calcium-potassium salt of HCA derived from Garcinia cambogia) in weight management. These studies also demonstrate that HCA-SX promotes fat oxidation, inhibits ATP-citrate lyase (a building block for fat synthesis), and lowers the level of leptin in obese subjects. Acute oral, acute dermal, primary dermal irritation and primary eye irritation toxicity studies have demonstrated the safety of HCA-SX. However, no long-term safety of HCA-SX or any other (-)-hydroxycitric acid extract has been previously assessed. In this study, we have evaluated the dose- and time-dependent effects of HCA-SX in Sprague-Dawley rats on body weight, hepatic and testicular lipid peroxidation, DNA fragmentation, liver and testis weight, expressed as such and as a % of body weight and brain weight, and histopathological changes over a period of 90 days. The animals were treated with 0, 0.2, 2.0 and 5.0% HCA-SX as feed intake and the animals were sacrificed on 30, 60 or 90 days of treatment. The feed and water intake were assessed and correlated with the reduction in body weight. HCA-SX supplementation demonstrated a reduction in body weight in both male and female rats over a period of 90 days as compared to the corresponding control animals. An advancing age-induced marginal increase in hepatic lipid peroxidation was observed in both male and female rats as compared to the corresponding control animals. However, no such difference in hepatic DNA fragmentation and testicular lipid peroxidation and DNA fragmentation was observed. Furthermore, liver and testis weight, expressed as such and as a percentage of body weight and brain weight, at 30, 60 and 90 days of treatment, exhibited no significant difference between the four groups. Taken together, these results indicate that treatment of HCA-SX over a period of 90 days results in a reduction in body weight, but did not cause any changes in hepatic and testicular lipid peroxidation, DNA fragmentation, or histopathological changes.

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Background: We recently reported that CD4+ T cells that have been activated in vivo or in vitro contain elevated cyclic adenosine monophosphate (cAMP) phosphodiesterase (PDE) activity. Since both phosphodiesterase inhibitors and glucocorticoids have anti-inflammatory activity, we sought to investigate the effect of beclomethasone on PDE activity. Methods: PDE activity was measured in CD4+ T cells after 24 h of culture with beclomethasone. Cells were obtained from the peripheral blood of nonatopic persons (nCells), pre-seasonal (pCells), seasonal (within the first 2 weeks; sCells) and mid-seasonal (mCells) allergic rhinitics and asymptomatic allergic asthmatics (aCells). In addition, the effect of beclomethasone on Th2 cell lines and cells that had been activated in vitro with PHA or interleukin (IL)-2 was determined. Results: PDE activity was decreased in a concentration-dependent manner by incubation of mCells, Th2 lines and PHA or IL-2-activated CD4+ T cells with beclomethasone (p < 0.05). However, beclomethasone did not modulate PDE activity in nCells, pCells, sCells, or aCells. Conclusions: Beclomethasone only decreases cAMP PDE activity in CD4+ T cells when it is increased by cell activation either in vitro or in vivo.

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