No abstract

This paper focuses on the effects of three thermal drying methods (microwave-, oven-and sun-drying) and one nonthermal drying method (freeze-drying) on the AOP of leaves of Vitex negundo and Vitex trifolia, which are consumed traditionally as herbal tea. Microwave-drying and freeze-drying were found to be able to maintain the AOP of the leaves but oven-drying and sun-drying resulted in deterioration of AOP. Microwave-drying has the advantage of short drying time and low water activity. AOP of Vitex herbal tea leaves that are microwave-dried and freeze-dried were not affected by storage up to 30 days. PRACTICAL APPLICATIONSTea, one of the most widely consumed beverages apart from water, has long been known for its health-promoting benefits in terms of its antioxidant properties due to its high phenolic content. Much of such studies, however, focus on green tea (Camellia sinensis). Although V. negundo and V. trifolia have been consumed traditionally as herbal tea, understanding of its antioxidant properties remains scarce. Drying serves as a vital part of tea processing, affecting its antioxidant content and appearance which in turn affects the commercial value of the tea. This study therefore serves as an important work in providing insights into the antioxidant properties of Vitex species and the best drying method of its leaves as herbal tea for commercial purpose. In addition, this study also provides insights into the effect of different drying methods on the storage of the leaves which is of value to the tea processing industry.

There is evidence that ATM mutated in ataxia-telangiectasia (A-T) plays a key role in protecting against mitochondrial dysfunction, the mechanism for which remains unresolved. We demonstrate here that ATM-deficient cells are exquisitely sensitive to nutrient deprivation, which can be explained by defective cross talk between the endoplasmic reticulum (ER) and the mitochondrion. Tethering between these two organelles in response to stress was reduced in cells lacking ATM, and consistent with this, Ca 2+ release and transfer between ER and mitochondria was reduced dramatically when compared with control cells. The impact of this on mitochondrial function was evident from an increase in oxygen consumption rates and a defect in mitophagy in ATM-deficient cells. Our findings reveal that ER-mitochondrial connectivity through IP3R1-GRP75-VDAC1, to maintain Ca 2+ homeostasis, as well as an abnormality in mitochondrial fusion defective in response to nutrient stress, can account for at least part of the mitochondrial dysfunction observed in A-T cells.

No abstract

Autosomal recessive ataxias are a clinically diverse group of syndromes that in some cases are caused by mutations in genes with roles in the DNA damage response, transcriptional regulation or mitochondrial function. One of these ataxias, known as Autosomal Recessive Cerebellar Ataxia Type-2 (ARCA-2, also known as SCAR9/COQ10D4; OMIM: #612016), arises due to mutations in the ADCK3 gene. The product of this gene (ADCK3) is an atypical kinase that is thought to play a regulatory role in coenzyme Q10 (CoQ10) biosynthesis. Although much work has been performed on the S. cerevisiae orthologue of ADCK3, the cellular and biochemical role of its mammalian counterpart, and why mutations in this gene lead to human disease is poorly understood. Here, we demonstrate that ADCK3 localises to mitochondrial cristae and is targeted to this organelle via the presence of an N-terminal localisation signal. Consistent with a role in CoQ10 biosynthesis, ADCK3 deficiency decreased cellular CoQ10 content. In addition, endogenous ADCK3 was found to associate in vitro with recombinant Coq3, Coq5, Coq7 and Coq9, components of the CoQ10 biosynthetic machinery. Furthermore, cell lines derived from ARCA-2 patients display signs of oxidative stress, defects in mitochondrial homeostasis and increases in lysosomal content. Together, these data shed light on the possible molecular role of ADCK3 and provide insight into the cellular pathways affected in ARCA-2 patients.