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This study investigated the effect of the catechins profile on the antioxidant activity of green tea extracts (GTEs) by comparing the antioxidant activity of an EGC-rich GTE (GTE1, catechin content: 58% EGC, 30.1% EGCG, 7.9% EC, and 3.9% ECG) and an EGCG-rich GTE (GTE2, catechin content: 60.6% EGCG, 17.7% EGC, 11.8% ECG, and 9.8% EC) in a DHA-rich oil. The effects of the individual catechins (EGC, EC, EGCG, and ECG) and reconstituted catechins mixtures (CatMix), prepared to contain the same amount of major catechins as in the GTEs, were also measured. All treatments (GTE1, CatMix1, GTE2, CatMix2, EGC250, EC250, EGCG250, and ECG250), each containing epistructured catechins at a concentration of 250 ppm, as well as the control (oil with no added antioxidant), were stored at 30 °C for 21 days with sampling intervals of 7 days. The antioxidant activity was assessed by measuring the peroxide value (PV) and p-anisidine value (p-AV) of oils. Changes in fatty acid content and catechins content were also monitored. Both GTEs enhanced the oxidative stability of the DHA-rich oil, but GTE1 demonstrated a stronger antioxidant activity than GTE2. No significant difference was observed between the PV of treatments with GTE1 and CatMix1 during storage, whereas the PV of oil with GTE2 was significantly higher than that with CatMix2 after 21 days. Among the individual catechins, EGC was the strongest antioxidant. Overall, the antioxidant activities of the extracts and catechins were observed in the decreasing order GTE1 ≈ EGC250 ≈ CatMix1 > GTE2 > EGCG250 ≈ CatMix2 > ECG250 > EC250. A significant change in fatty acid content was observed for the control and EC250 samples, and the catechins were most stable in GTE1-supplemented oil. Our results indicate that the EGC-rich GTE is a more potent antioxidant in DHA-rich oil than the EGCG-rich GTE.

Cancer research has benefited immensely from the use of animal models. Several genetic tools accessible in rodent models have provided valuable insight into cellular and molecular mechanisms linked to cancer development or metastasis and various lines are available. However, at the same time, it is important to accompany these findings with those from alternative or non-model animals to offer new perspectives into the understanding of tumor development, prevention, and treatment. In this review, we first discuss animals characterized by little or no tumor development. Cancer incidence in small animals, such as the naked mole rat, blind mole rat and bats have been reported as almost negligible and tumor development may be inhibited by increased defense and repair mechanisms, altered cell cycle signaling and reduced rates of cell migration to avoid tumor microenvironments. On the other end of the size spectrum, large animals such as elephants and whales also appear to have low overall cancer rates, possibly due to gene replicates that are involved in apoptosis and therefore can inhibit uncontrolled cell cycle progression. While it is important to determine the mechanisms that lead to cancer protection in these animals, we can also take advantage of other animals that are highly susceptible to cancer, especially those which develop tumors similar to humans, such as carnivores or poultry. The use of such animals does not require the transplantation of malignant cancer cells or use of oncogenic substances as they spontaneously develop tumors of similar presentation and pathophysiology to those found in humans. For example, some tumor suppressor genes are highly conserved between humans and domestic species, and various tumors develop in similar ways or because of a common environment. These animals are therefore of great interest for broadening perspectives and techniques and for gathering information on the tumor mechanisms of certain types of cancer. Here we present a

Plant-derived conjugated linolenic acids (CLnA) have been widely studied for their preventive and therapeutic properties against diverse diseases such as cancer. In particular, punicic acid (PunA), a conjugated linolenic acid isomer (C18:3 c9t11c13) present at up to 83% in pomegranate seed oil, has been shown to exert anti-cancer effects, although the mechanism behind its cytotoxicity remains unclear. Ferroptosis, a cell death triggered by an overwhelming accumulation of lipid peroxides, has recently arisen as a potential mechanism underlying CLnA cytotoxicity. In the present study, we show that PunA is highly cytotoxic to HCT-116 colorectal and FaDu hypopharyngeal carcinoma cells grown either in monolayers or as three-dimensional spheroids. Moreover, our data indicate that PunA triggers ferroptosis in carcinoma cells. It induces significant lipid peroxidation and its effects are prevented by the addition of ferroptosis inhibitors. A combination with docosahexaenoic acid (DHA), a known polyunsaturated fatty acid with anticancer properties, synergistically increases PunA cytotoxicity. Our findings highlight the potential of using PunA as a ferroptosis-sensitizing phytochemical for the prevention and treatment of cancer.

The increase in global life expectancy continues to grow, with predictions that individuals over the age of 60 will reach 2 billion by 2050. In light of this, we must consider that elderly individuals are at a higher risk of encountering age-related diseases including those that are difficult to treat. Improving health later in life is an important objective to avoid social and economic challenges. The physiological dysfunction and increased susceptibility to disease that accompany aging are often due to a decrease in the functionality and resilience of key cell types in the body. Decline in mitochondrial function can be one of the triggers of cellular aging, and therefore one of the causes of the detrimental effects of aging. It may be difficult to link the function of a small cellular organelle to the overall function of the body, but mitochondria are the main source of cellular energy. Mitochondrial function relies on over 1000 proteins, most of which are encoded within the nucleus and imported from the cytosol. Among these, are DNA methyltransferases, enzymes that participate in DNA epigenetic modifications. Although, DNA epigenetic regulation in the mitochondria is still a controversial subject, mounting evidence suggests that it plays an important role in mitochondrial function. Therefore, the main goal of the research program is to determine how mitochondrial protein import and specifically the import of DNA methyltransferase into mitochondria, ultimately affect mitochondrial function, in an aging organism. To pursue this goal, African turquoise killifish will be use as the main experimental model. This fish is currently the shortest living vertebrate in captivity. They offer the advantage of short lifespans associated with invertebrate models while maintaining many aging characteristics reported in classical vertebrate models as well as humans. Together, these features have made this animal one of the most interesting models in the field of aging research. W

Sexual dimorphism is observed at the beginning of embryonic development. At this stage, it is mainly due to the overexpression of X-linked genes in female embryos. This early transcriptional dimorphism leads to differences in metabolism and environmental adaptations between the sexes. Our objective was to study the impact of induced oxidative stress on in vitro bovine embryos produced in two conditions (with or without serum), considering the embryo sex. Two stress inducers were used, each having a different mode of action: AAPH and menadione, which produces reactive oxygen species (ROS) in the culture medium or elevates intracellular ROS production, respectively. We assessed the sex ratio of embryos that reached the blastocyst stage as well as two quality markers: total cell number and apoptotic rates. Male embryos were more resistant against oxidative stress when cultured in presence of serum, regardless of the treatment. In contrast, female embryos were more resistant when cultured in serum-free medium following AAPH treatment, while exposure to menadione had no impact on sex ratio. The same trends were observed on the quality parameters of embryos that have reached the blastocyst stage. In order to understand the origin of the observed differences, the expression of six genes implicated in REDOX status regulation or apoptosis were evaluated by RT-qPCR on single blastocysts in the above conditions, and included X-linked (AIFM1, G6PD, HPRT and XIAP) and autosomal genes (BAX and GAPDH). This study confirmed the overexpression of X-linked genes in female embryos and highlighted differences between media for the response of embryos to oxidative stress, opening new research perspectives in order to improve our knowledge of the environmental impact on early sexual dimorphism., Un dimorphisme sexuel est observé dès le début du développement. À ce stade, il est surtout dû à une surexpression des gènes du chromosome X chez les femelles. Ce dimorphisme transcriptionnel précoce mène à des différences métaboliques et d’adaptation à l’environnement entre sexes. Notre objectif était d’étudier l’impact d’un stress oxydant induit sur des embryons bovins produits in vitro dans deux conditions (avec et sans sérum) en tenant compte du sexe de l’embryon. Deux inducteurs de stress oxydant possédant des modes d’action différents ont été utilisés : l’AAPH, qui produit des espèces réactives de l’oxygène (ROS) dans le milieu, et la ménadione qui augmente la production de ROS intracellulaires. Nous avons évalué le sex-ratio des embryons qui ont atteint le stade blastocyste, ainsi que deux critères de qualité, le nombre de cellules et le taux de cellules apoptotiques. Alors que les embryons mâles résistent mieux au stress en présence de sérum, quel que soit l’inducteur, les embryons femelles survivent mieux dans le milieu sans sérum lorsque le stress est induit par l’AAPH, tandis que la ménadione n’a pas d’effet sur le sex-ratio des embryons. L’impact sur la qualité des blastocystes tend à aller dans le même sens. Pour comprendre l’origine des différences observées, l’expression de 6 gènes impliqués dans la régulation de l’équilibre REDOX ou de l’apoptose a été étudiée par RT-qPCR sur blastocystes individuels dans les mêmes conditions : 4 gènes liés au X (AIFM1, G6PD, HPRT et XIAP) et 2 gènes autosomaux (BAX et GAPDH). Cette étude a confirmé la surexpression des gènes liés au X chez les embryons femelles et a mis en évidence des différences entre milieux pour la réponse des embryons au stress oxydant, ouvrant de nouvelles pistes d’investigation pour mieux comprendre l’impact des conditions environnementales sur le dimorphisme sexuel précoce., (SC - Sciences) -- UCL, 2019