Molecular mechanisms of steroid hormone action

The generation of DNA double strand breaks (DSBs) in UV-irradiated cells, specifically in replicating DNA, has been known for a long time [ 86 ]. DNA strand breaks are observed extensively in cells under UV-B irradiation [ 87 , 88 ]. UV-B-induced ROS [ 89 ] as well as DNA lesions (CPDs and 6-4PPs) may cause primary as well as secondary breaks, respectively. These lesions are commonly associated with transcription/replication blockage that may lead to production of DNA double-strand breaks (DSBs) at the sites of collapsed replication forks of CPDs-containing DNA [ 90 , 91 ] (Figure 8 ). Dunkern and Kaina [ 92 ] also observed UV-C-induced DNA DSBs, arising from replication of damaged DNA. A significantly low amount of DSBs was found in the cell where replication was inhibited. It was assumed that initial photoproducts are converted into DSBs during DNA replication, due to not a distinct process, that is, “collapse of replication forks” [ 93 ]. After labeling of replicating DNA of UV-irradiated SV40-transformed human cell lines with radioactive precursors, an increased number of DSBs was observed in NER deficient cells in comparison to NER proficient cells. These results further support the view that DSBs are produced during the replication of unrepaired UV-induced DNA lesions [ 91 ]. DSBs can be formed in response to the repair of single strand breaks (SSBs) passing through base excision repair (BER) [ 94 , 95 ]. Overall, it seems that UV radiation does not directly produce DNA DSBs but rather produces pyrimidine dimers and other photoproducts leading to replication arrest and DSBs. UV-induced replication arrest in the xeroderma pigmentosum variant (XPV) followed by the accumulation of Mre11/Rad50/Nbs1 complex and phosphorylated histone H2AX ( γ -H2AX) in large nuclear foci at sites of stalled replication forks also suggests that UV damage leads to the formation of DSBs during the course of replication arrest [ 90 , 95 ].

In November 1949, with the seminal paper, " Sickle Cell Anemia, a Molecular Disease ", [3] in Science magazine, Linus Pauling , Harvey Itano and their collaborators laid the groundwork for establishing the field of molecular medicine. [4] In 1956, Roger J. Williams wrote Biochemical Individuality , [5] a prescient book about genetics, prevention and treatment of disease on a molecular basis, and nutrition which is now variously referred to as individualized medicine [6] and orthomolecular medicine . [7] Another paper in Science by Pauling in 1968, [8] introduced and defined this view of molecular medicine that focuses on natural and nutritional substances used for treatment and prevention.

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Aging represents a physiological and per se non-pathological and multifactorial process involving a set of key genes and mechanisms being triggered by different endogenous and exogenous factors. Since aging is a major risk factor in connection with a variety of human disorders, it is increasingly becoming a central topic in biochemical and medical research. The plethora of theories on aging – some of which have been discussed for decades – are neither isolated nor contradictory but instead can be connected in a network of pathways and processes at the cellular and molecular levels. This book summarizes the most prominent and important approaches, focusing on telomeres, DNA damage and oxidative stress as well as on the possible role of nutrition, the interplay between genes and environment (epigenetics) and intracellular protein homeostasis and introduces some genes that have actually extended life spans in animal models. Linking these different determinants of aging with disease, this volume aims to reveal their multiple interdependencies. We see that there is no single “perfect” theory of aging and that instead it is possible to define what the authors call the molecular aging matrix of the cell. A better knowledge of its key mechanisms and the mutual connections between its components will lead to a better understanding of age-associated disorders such as Alzheimer’s disease.

Molecular mechanisms of steroid hormone action

molecular mechanisms of steroid hormone action

Aging represents a physiological and per se non-pathological and multifactorial process involving a set of key genes and mechanisms being triggered by different endogenous and exogenous factors. Since aging is a major risk factor in connection with a variety of human disorders, it is increasingly becoming a central topic in biochemical and medical research. The plethora of theories on aging – some of which have been discussed for decades – are neither isolated nor contradictory but instead can be connected in a network of pathways and processes at the cellular and molecular levels. This book summarizes the most prominent and important approaches, focusing on telomeres, DNA damage and oxidative stress as well as on the possible role of nutrition, the interplay between genes and environment (epigenetics) and intracellular protein homeostasis and introduces some genes that have actually extended life spans in animal models. Linking these different determinants of aging with disease, this volume aims to reveal their multiple interdependencies. We see that there is no single “perfect” theory of aging and that instead it is possible to define what the authors call the molecular aging matrix of the cell. A better knowledge of its key mechanisms and the mutual connections between its components will lead to a better understanding of age-associated disorders such as Alzheimer’s disease.

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