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Articles by R.G. Ahmed
Total Records ( 4 ) for R.G. Ahmed
  O.M. Ahmed , R.G. Ahmed , M.M.S. Nada and M. Bahgat
  Because the heat stress is one of the most stressful factors on the biological systems, it was important to study its effect on the development of neurons in different Central Nervous System (CNS) regions of albino rat newborns. Development of neurons in cerebral cortex, cerebellar cortex and cervical and lumbar regions of the spinal cord was followed by using Golgi-copsch stain between days 7 and 21 after birth. The present study does not only illustrate the aspects of development processes of normal neurons in different regions of CNS, but also records the effects of heat stress (40±1°C) on them. The present study revealed that the development of the CNS is extremely sensitive to heat stress which led, in turn, to some harmful effects on the neurons development and caused delay of the dendritic arborization in all investigated CNS regions of the rat newborns. Taken together, further studies are required to determine if the beneficial effects of heat exposure result in changes of stress complications only or not. Thus, experiments will be required to solve these problems and to comprehend the actual role of heatstroke in neurodegeneration of CNS.
  R.G. Ahmed
  The number of reports on the effects of various types of radiation is gradually increasing because of weakening of the immune system. Radiation can penetrate into living cells and result in the transfer of radiation energy to the biological material. The absorbed energy can increase the reactive oxygen species and break chemical bonds and cause ionization of different biologically essential macromolecules, such as DNA membrane lipids and proteins. Damage to the cellular membrane release the hydrolytic enzymes responsible for various catabolic processes in the tissues and leads to cell death. An understanding of the pattern in critical cellular structures such as DNA is an important prerequisite for a mechanistic assessment of primary radiation injury. The DNA damage induced by radiation such as base alterations, cross linking, strands breaker chromosomal aberration which may in turn lead to mutations. In order to further explore the harmful effects of radiation. I have produced a variety of effects of radiation on the apoptosis and necrosis. Indeed, the present review has shown that the increase in the oxidative stress (increased endogenous production of the free radicals) due to radiation may be a reason for such a damage of the cell membrane, and may lead to harming the cellular elements (such as DNA). Here, one can hypothesize that, the cells with increased sensitivity to oxidative stress may be more susceptible to damage by radiation compared to normal cells. The ultimate biological consequences of this effect are subsequently processed by these cells. Much work remains to be done to firmly establish this concept.
  R.G. Ahmed
  The number of reports on the effects of temperature is still increasing because of the temperature is one of the most encountered stressful factors in the environment, thus it deemed important to survey the literatures for effects of temperature on the biological consequences. The objective of this review was to establish the thermoregulatory response and adaptation of some non-mammalian species during temperature. Although, there was relative scarcity of information on the relation between oxidative stress and antioxidant enzymes during temperature, this review great interest to elicit this relation in non-mammalian species. Here, this review suggests that, the increase in the oxidative stress due to temperature may be a reason for such decrease and exhaustion of antioxidant enzymes and a sequence of cellular injury or death, because of increased endogenous production of the free radicals. However, there was exception in this hypothesis because this argument is still ambiguous because of the difficulties of the direct observation of the active oxygen species in the biological systems due to their short lifetime. Taken together, because of one of the most important functions of heat shock protein is to protect the organisms from the deleterious effects of temperature, thus, it can be hypothesized that the formation of heat shock protein and antioxidant enzymes may be related to the changes in the levels of free radicals in non-mammalian species during temperature.
  R.G. Ahmed , Yuan Ye Ma and S.H. Lee
  Peroxiredoxins (Prxs) are a family of novel antioxidant proteins that are found in a variety of species and participate in a number of vital biological processes such as proliferation, differentiation, response to oxidative stress and intracellular signaling. It has been proposed that they might participate in these cellular processes by playing a role in eliminating or regulating the intracellular concentration of peroxides produced during metabolism as well as in the signaling cascades of growth factors and cytokines. Mammalian cells express six isoforms of Prx (Prx I to VI), which are classified into three subgroups (typical 2-Cys, atypical 2-Cys and 1-Cys) based on the number and position of cysteine (Cys) residues that participate in catalysis and on amino acid sequences and the immunological reactivity. Members of the typical 2-Cys subgroup include Prx I through Prx IV and contain an additional conserved cysteine in the carboxyl-terminal region, whereas Prx V and Prx VI, members of the atypical 2-Cys and 1-Cys subgroups, respectively, do not contain this second conserved Cys. On the other hand, Prxs activity can be regulated by phosphorylation and proteolysis processes in addition to overoxidation. Taken together, this study suggest that the generation of the oxidative stress which caused neurodegeneration may couple with produced Prxs and the reverse is true. However, this argument is still unclear on account of the difficulties of the direct observation of the reactive oxygen species due to their biological lifetime is short. Thus, experiments will be required to solve these problems and to comprehend the actual role of Prxs in neurodegeneration.
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