Supplementation with Achyrocline satureioides Inflorescence Extracts to Pregnant and Breastfeeding Rats Induces Tissue-Specific Changes in Enzymatic Activity and Lower Neonatal Survival.

Achyrocline satureioides (AS, family Asteraceae) is a plant widely used in traditional medicine for stomach, digestive, and gastrointestinal disorders during pregnancy. Studies regarding the indiscriminate use of plant infusions during pregnancy are limited. Recent reports have shown that chronic flavonoid supplementation induces toxicity in vivo and raises the mortality rates of healthy subjects. Therefore, we investigated whether supplementation of pregnant and lactating Wistar rats with two AS inflorescence extracts, consisting of an aqueous (AQ) extract similar to a tea (47 mg·kg-1·day) and a hydroethanolic (HA) extract (35 mg·kg-1·day-1) with a higher flavonoid content, could induce redox-related side effects. Total reactive antioxidant potential (TRAP), thiobarbituric reactive species (TBARS), and total reduced thiol (SH) content were evaluated. Superoxide dismutase (SOD) and catalase (CAT) activities were additionally quantified. Our data suggest that both AQ and HA of AS inflorescence extracts may induce symptoms of toxicity in concentrations of (47 mg·kg-1·day) and (35 mg·kg-1·day-1), respectively, in mothers regarding the delivery index and further decrease of neonatal survival. Of note, significant tissue-specific changes in maternal (liver, kidney, heart, and hippocampus) and pups (liver and kidney) biochemical oxidative parameters were observed. Our findings provide evidence that may support the need to control supplementation with the AQ of AS inflorescence extracts during gestation due to potential toxicity in vivo, which might be related, at least in part, to changes in tissue-specific redox homeostasis and enzymatic activity.

Chronic retinyl palmitate supplementation to middle-aged Wistar rats disrupts the brain redox homeostasis and induces changes in emotional behavior.

SCOPE: Aging process makes older adults especially vulnerable to neurodegeneration and mental disorders. Overconsumption-related neurotoxic effects of certain dietary nutrients by older population could represent a contribution factor for the development of neuropsychiatric conditions by this subpopulation. Thus, we here investigated whether chronic supplementation with retinyl palmitate, at doses commonly found in vitamin supplements (300, 600, and 3000 mcg of RAE/kg/day), could have an impact on emotional behavior of middle-aged Wistar rats. METHODS AND RESULTS: We report that supplementation with retinyl palmitate for 28 days induces an altered emotional state of middle-aged Wistar rats and oxidative stress in cerebellum, cerebral cortex, hippocampus, and striatum, associated with imbalance of enzymatic antioxidant defenses, decrease in non-enzymatic antioxidant defenses, and increase in protein and lipid damages. CONCLUSION: Our data show evidence for (i) changes in emotional reactivity, similar to anxiety, in middle-aged rats chronically supplemented with retinyl palmitate; and (ii) suggest a possible interrelation between pro-oxidant events in the brain and these differences in the behavioral profile that cannot be attributed to hepatotoxicity. Our results invite for additional studies to further investigate such interrelation.

Supplementation of adult rats with moderate amounts of ß-carotene modulates the redox status in plasma without exerting pro-oxidant effects in the brain: a safer alternative to food fortification with vitamin A?

Despite the antioxidant potential of vitamin A, recent studies reported that chronic retinol ester supplementation can also exert pro-oxidant effects and neurotoxicity in vivo and raises the mortality rates among healthy subjects. Our aim was to find evidence for a safer (i.e., less toxic) molecule with provitamin A activity. Therefore, we investigated whether chronic supplementation of healthy Wistar rats with ß-carotene (0.6, 3, and 6 mg/kg/day) would demonstrate antioxidant characteristics without leading to pro-oxidant side effects in the brain. Total reactive antioxidant potential (TRAP), thiobarbituric reactive species level (TBARS), and total reduced thiol content (SH) were evaluated in plasma. TBARS and SH were additionally evaluated in selected brain regions together with superoxide dismutase (SOD) and catalase (CAT) activity. In the present study, we show that ß-carotene is able to exert antioxidant activity in plasma without triggering pro-oxidant events in the brain, providing evidence that may justify its further evaluation as a safer nutritional supplement with provitamin A activity.

Guarana (Paullinia cupana Mart.) prevents ß-amyloid aggregation, generation of advanced glycation-end products (AGEs), and acrolein-induced cytotoxicity on human neuronal-like cells.

Advanced glycation end-products (AGEs) are considered potent molecules capable of promoting neuronal cell death and participating in the development of neurodegenerative disorders such as Alzheimer's disease (AD). Previous studies have shown that AGEs exacerbate ß-amyloid (Aß) aggregation and AGE-related cross-links are also detected in senile plaques. Acrolein (ACR) is an α, ß-unsaturated aldehyde found in the environment and thermally processed foods, which can additionally be generated through endogenous metabolism. The role of ACR in AD is widely accepted in the literature. Guarana (Paullinia cupana Mart.) is popularly consumed by the population in Brazil, mainly for its stimulant activity. In the present study, we showed that guarana (10, 100, and 1000 µg/mL) is able to prevent protein glycation, ß-amyloid aggregation, in vitro methylglyoxal, glyoxal, and ACR (20 µM)-induced toxicity on neuronal-like cells (SH-SY5Y). Since these are considered typical AD pathological hallmarks, we propose that guarana may deserve further research as a potential therapeutic agent in such a neurodegenerative disease.