Pyrophosphatase, Peroxidase and Polyphenoloxidase Activities during Leaf Development and Senescence

Inorganic pyrophosphatase, peroxidase, and polyphenoloxidase activities were studied as the function of leaf insertion level in eight monocotyledonous and eight dicotyledonous species. Alkaline inorganic pyrophosphatase shows a declining activity toward the end of senescence whereas no regular drift in either peroxidase or polyphenoloxidase activities was noticed during senescence of attached leaves. In the primary leaves of rice, peroxidase and polyphenoloxidase activities were high in the senescent leaves and there exists a correlation between chlorophyll content and peroxidase activity though not with polyphenoloxidase activity. Upon detachment leaves exhibit increasing peroxidase and polyphenoloxidase activities with time. The distribution of the enzyme activities during senescence of attached leaves is suggested to be species-specific, and an increase in peroxidase and polyphenoloxidase activities cannot be taken as an indicator of leaf senescence.     

The Behaviour of Peroxidase and Polyphenol Oxidase during the Growth and Senescence of Tobacco Leaves

The activities of polyphenol oxidase and peroxidase per unitarea of attached tobacco leaves increased as the leaves expanded,and reached a stable level in the mature leaves. After the onsetof senescence the enzyme activities fell rapidly, but at a laterstage they showed a small rise. Enzyme activities in tissuestaken from non-senescent leaves increased during incubationat 20 °C. These increases were sensitive to inhibitors ofprotein synthesis. Enzyme activities in tissues taken from leavesin early senescence increased during incubation at 35 °Cbut not at 20 °C. These increases were very largely insensitiveto inhibitors of protein synthesis and were not apparently relatedto de novo protein synthesis. There were no increases in enzymeactivities in tissues taken from leaves in late senescence andincubated at 35 °C or 20 °C.     

四种叶菜衰老期间呼吸、乙烯产生、IAA和过氧化物酶的变化及其相互关系

结球白菜、结球甘蓝和菠菜在衰老期间的呼吸强度逐渐上升,后期下降,呈有峰型变化,而结球生菜的呼吸强度随衰老而下降,呈无峰型变化。外源乙烯使前三者的呼吸峰提前,但不改变其变化趋势,使后者出现呼吸峰。衰老期间内源乙烯均上升;过氧化物酶活力增加,IAA含量下降,两者存在极显著负相关。幼叶乙烯生成与IAA含量相关,老叶乙烯生成不受IAA水平影响。     

Leaf Senescence and GABA Shunt

Leaf senescence is highly regulated and complex developmental process that involves degradation of macromolecules as well as its recycling. Senescence process involves loss of chlorophyll, degradation of proteins, nucleic acid, lipid and mobilization of nutrients through its transport to the growing parts, developing fruits and seeds. Nitrogen is the most important nutrient to be recycled in senescence process. GABA-transaminase (γ-aminobutyric acid) is found to play very important role in nitrogen recycling process through GABA-shunt. Therefore, it is of interest to review the significance of GABA shunt in leaf senescence.     

端粒位置效应与人类衰老

端粒随细胞分裂进行性缩短不但防止了人类肿瘤的发展,而且与人类的衰老密切相关。另外,端粒中存在一种特殊的现象：端粒位置效应,它首先在酵母中发现,表现为靠近端粒序列附近的基因表达因端粒的位置效应而沉默。在人类细胞中也存在端粒位置效应,并且有多种因子参与此效应,它可能对细胞生长停止、肿瘤以及衰老发生时等许多随端粒缩短密切相关基因的程序性表达产生重要作用。     

植物叶片衰老与氧化胁迫

叶片衰老是叶片生长发育进程中的最后阶段,与活性氧伤害有着密切的关系。介绍了植物叶片衰老过程中活性氧产生及清除系统的变化,讨论了对水分胁迫与氧化胁迫的交叉抗性,并对下一步的研究作出了展望     

Senescence and epigenetic dysregulation in cancer

Mammalian cells have a finite proliferative lifespan, at the end of which they are unable to enter S phase in response to mitogenic stimuli. They undergo morphological changes and synthesize an altered repertoire of cell type-specific proteins. This non-proliferative state is termed replicative senescence and is regarded as a major tumor suppressor mechanism. The ability to overcome senescence and obtain a limitless replicative potential is called immortalization, and considered to be one of the prerequisites of cancer formation. While senescence mainly represents a genetically governed process, epigenetic changes in cancer have received increasing attention as an alternative mechanism for mediating gene expression changes in transformed cells. DNA methylation of promoter-containing CpG islands has emerged as an epigenetic mechanism of silencing tumor suppressor genes. New insights are being gained into the mechanisms causing aberrant methylation in cancer and evidence suggests that aging is accompanied by accumulation of cells with aberrant CpG island methylation. Aberrant methylation may contribute to many of the physiological and pathological changes associated with aging including tumor development. Finally, we describe how genes involved in promoting longevity might inhibit pathways promoting tumorigenesis.     

Senescence, aging, and disease

All over the world people are surviving into their seventh and later decades of life more frequently today than ever before in human history. Some remain in good health, while others show chronic degenerative conditions (CDCs), frailty, and relatively rapid mortality. Thereafter, multiple factors promoting health and well-being become ever more complex as we age. After attainment of reproductive maturation, many physiological decrements occurring in concert with age reflect both senescent and disease processes, not simply the passage of time. Senescence is a process that begins with DNA, molecules and cells and ultimately terminates in cellular death, loss of organ function, and somatic frailty. These changes are different from benign changes with age that do not alter function. Both differ from the pathological processes represented by disease. Either disease or senescence may be age-related, but neither is age-determined. Disease results from pathological alterations and it affects all age groups. Diseases need not be related to senescence, which includes alterations due to inherent aspects of organismal biology. Distinctions among senescence, aging, and disease blur for the late-life CDCs because, in addition to disease processes, many CDCs are phenotypic manifestations of senescing DNA, organelles, cells, and organs. During earlier epochs of human evolution, greater environmental exposures and fewer cultural buffers likely lead to greater frailty and mortality before senescence progressed greatly, as they still do for most animals. In modern-day settings, culturally patterned behaviors have allowed human frailty to become disconnected somewhat from mortality, unlike non-human species.