Under normal physiological conditions, reactive oxygen species (ROS) serve as 'redox messengers' in the regulation of intracellular signalling, whereas excess ROS may induce irreversible damage to cellular components and lead to cell death by promoting the intrinsic apoptotic pathway through mitochondria. In the aging process, accumulation of mitochondria DNA mutations, impairment of oxidative phosphorylation as well as an imbalance in the expression of antioxidant enzymes result in further overproduction of ROS. This mitochondrial dysfunction-elicited ROS production axis forms a vicious cycle, which is the basis of mitochondrial free radical theory of aging. In addition, several lines of evidence have emerged recently to demonstrate that ROS play crucial roles in the regulation of cellular metabolism, antioxidant defence and posttranslational modification of proteins. We first discuss the oxidative stress responses, including metabolites redistribution and alteration of the acetylation status of proteins, in human cells with mitochondrial dysfunction and in aging. On the other hand, autophagy and mitophagy eliminate defective mitochondria and serve as a scavenger and apoptosis defender of cells in response to oxidative stress during aging. These scenarios mediate the restoration or adaptation of cells to respond to aging and age-related disorders for survival. In the natural course of aging, the homeostasis in the network of oxidative stress responses is disturbed by a progressive increase in the intracellular level of the ROS generated by defective mitochondria. Caloric restriction, which is generally thought to promote longevity, has been reported to enhance the efficiency of this network and provide multiple benefits to tissue cells. In this review, we emphasize the positive and integrative roles of mild oxidative stress elicited by mitochondria in the regulation of adaptation, anti-aging and scavenging pathway beyond their roles in the vicious cycle of mitochondrial dysfunction in the aging process.
Viral infections are a major global health issue, but no current method allows rapid, direct, and ultrasensitive quantification of intact viruses with the ability to inform infectivity, causing misdiagnoses and spread of the viruses. Here, we report a method for direct detection and differentiation of infectious from noninfectious human adenovirus and SARS-CoV-2, as well as from other virus types, without any sample pretreatment. DNA aptamers are selected from a DNA library to bind intact infectious, but not noninfectious, virus and then incorporated into a solid-state nanopore, which allows strong confinement of the virus to enhance sensitivity down to 1 pfu/ml for human adenovirus and 1 × 10 4 copies/ml for SARS-CoV-2. Applications of the aptamer-nanopore sensors in different types of water samples, saliva, and serum are demonstrated for both enveloped and nonenveloped viruses, making the sensor generally applicable for detecting these and other emerging viruses of environmental and public health concern.
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