CHANGES IN PHOTOSYNTHESIS IN RESPONSE TO COMBINED IRRADIANCE AND TEMPERATURE STRESS IN CYANOBACTERIAL SURFACE WATERBLOOMS1

Buoyant cyanobacteria, previously mixed throughout the water column, float to the lake surface and form a surface waterbloom when mixing subsides. At the surface, the cells are exposed to full sunlight, and this abrupt change in photon irradiance may induce photoinhibition; at the same time, temperature rises as well. This study investigated the damaging effects of this increase in temperature as well as the ecologically more relevant combination of both an increased temperature and a high photon irradiance. Analysis of surface blooms with oxygen microelectrodes showed that integrated oxygen contents that are dependent on the balance of photosynthetic oxygen evolution and respiratory oxygen uptake decreased when temperature was raised above the lake temperature. Gross rates of photosynthesis were unaffected by temperatures up to of 35°C; hence, a moderate increase in temperature mainly stimulated oxygen uptake. Preincubation of cells of the cyanobacterium Anabaena flos-aquae (Lyngb.) de Brébisson at temperatures up to 35°C did not affect the subsequent measurement of rates of net photosynthesis. Another 5°C rise in temperature severely damaged the photosynthetic apparatus. Failure to restore net rates of photosynthesis was coupled to a strong quenching of the ratio of variable to maximum fluorescence, F_v/F_m, that was the result of a rise in F_o. A combination of high temperature and high photon irradiance was more damaging than high temperature alone. In contrast, low photon irradiances offered substantial protection against heat injury of the photosynthetic apparatus. I conclude from this study that because cyanobacteria usually are acclimated to low average irradiance prior to bloom formation, there is a reasonable risk of chronic photoinhibition. The increase in temperature will enhance the photodamage of cells in the top layer of the bloom. Low photon irradiances in subsurface layers will offer protection against heat injury. If the high temperatures extend to the deepest, dark layers of the bloom, damage in those layers is likely to occur.     

Flooding-induced membrane damage, lipid oxidation and activated oxygen generation in corn leaves

Flooding effects on membrane permeability, lipid peroxidation and activated oxygen metabolism in corn (Zea mays L.) leaves were investigated to determine if activated oxygens are involved in corn flooding-injury. Potted corn plants were flooded at the 4-leaf stage in a controlled environment. A 7-day flooding treatment resulted in a significant increase in chlorophyll breakdown, lipid peroxidation (malondialdehye content), membrane permeability, and the production of superoxide (O ₂ ^- ) and hydrogen peroxide (H₂O₂) in corn leaves. The effects were much greater in older leaves than in younger ones. Spraying leaves with 8-hydroxyquinoline (an O ₂ ^- scavenger) and sodium benzoate (an .OH scavenger) reduced the oxidative damage and enhanced superoxide dismutase (SOD) activity. A short duration flooding treatment elevated the activities of SOD, catalase, ascorbate peroxidase (AP), and glutathione reductase (GR), while further flooding significantly reduced the enzyme activities but enhanced the concentrations of ascorbic acid and reduced form glutathione (GSH). It was noted that the decline in SOD activity was greater than that in H₂O₂ scavengers (AP and GR). The results suggested that O ₂ ^- induced lipid peroxidation and membrane damage, and that excessive accumulation of O ₂ ^- is due to the reduced activity of SOD under flooding stress.     

Effect of maximal arm exercise on skin blood flux in the paralyzed lower limbs in persons with spinal cord injury

The purpose of the present study was to examine the effect of maximal arm exercise on the skin blood circulation of the paralyzed lower limbs in persons with spinal cord injury (PSCI). Eight male PSCI with complete lesions located between T3 and L1 performed graded maximal arm-cranking exercise (MACE) to exhaustion. The skin blood flux at the thigh (SBFT) and that at the calf (SBFC) were monitored using laser-Doppler flowmeter at rest and for 15 s immediately after the MACE. The subject's mean peak oxygen uptake and peak heart rate was 1.41 ± 0.22 1·min⁻¹ and 171.6 ± 19.2 beats·min⁻¹, respectively. No PSCI showed any increase in either SBFT or SBFC after the MACE, when compared with the values at rest. These results suggest that the blood circulation of the skin in the paralyzed lower limbs in PSCI is unaffected by the MACE.     

细胞寒害的热力学熵理论(Ⅱ)──超熵产生作为寒害稳定性判据的理论研究

本文从物质和能量交换的角度,运用非平衡态热力学超熵产生理论,分析了寒害定态的稳定性,并建立了超熵产生判据．理论分析所得的结论与实验结果基本相符．     

毛喉萜对人胃癌细胞BGC－823中蛋白激酶C及其亚类的影响

以人胃癌细胞ＢＧＣ－８２３为模型,研究了毛喉萜（ｆｏｒｓｋｏｌｉｎ）对胃癌细胞中蛋白激酶Ｃ活性及其亚类基因表达的作用,同时也观察了毛喉萜对癌基因ｃ－ｊｕｎ及抑癌基因ｐ５３表达的影响．结果表明,２×１０~（－５）ｍｏｌ／Ｌ毛喉萜处理ＢＧＣ－８２３细胞７２ｈ,细胞质、膜和细胞核ＰＫＣ活性下降,ＰＫＣ亚类β,γ基因表达被抑制,癌基因ｃ－ｊｕｎ的表达也明显降低,而抑癌基因ｐ５３表达升高,上述变化可能是毛喉萜抑制胃癌细胞增殖等生理效应的重要分子事件。     

Axenic Cultivation of Entamoeba dispar Brumpt 1925, Entamoeba insolita Geiman and Wichterman 1937 and Entamoeba ranarum Grassi 1879

ABSTRACT. Three species of Entamoeba have been grown in axenic culture for the first time. In two cases, novel methods for adapting the organisms to growth without bacteria were employed. While E. ranarum was axenized by the classic technique of Diamond, from a monoxenic culture with Trypanosoma cruzi as the associate, both E. dispar and E. insolita were first grown in axenic culture medium supplemented with lethally irradiated bacteria. From there, E. insolita was axenized directly, but E. dispar initially required the presence of fixed bacteria. After prolonged culture under this technically axenic but unwieldy culture system, E. dispar was eventually adapted to growth in the absence of added bacteria.     

[125I]CGP 42112 reveals a non-angiotensin II binding site in 1-methyl-4-phenylpyridine (MPP+)-induced brain injury

Summary 1. Intracerebral injection of the oxidative metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), 1-methyl-4-phenylpyridine (MPP⁺), into the substantia nigra of adult rats resulted in a lesion at the injection site.2. Using autoradiography, we localized specific [¹²⁵]CGP 42112 binding that was not recognized by angiostensin II or angiotensin II AT₁ or AT₂ receptorselective ligands.3. Our results suggest that [¹²⁵I]CGP 42112 may be binding to activated microglia that appear at the lesion site.     

Enhanced Phosphodiestric Breakdown of Phosphatidylinositol Bisphosphate After Experimental Brain Injury

Abstract: Regional levels of lactate and inositol 1,4,5-trisphosphate (IP₃), a cellular second messenger of the excitatory neurotransmitter system, were measured after lateral fluid percussion (FP) brain injury in rats. At 5 min postinjury, tissue lactate concentrations were significantly elevated in the cortices and hippocampi of both the ipsilateral and contralateral hemispheres. By 20 min postinjury, lactate concentrations were elevated only in the cortices and hippocampus of the ipsilateral hemisphere. Whereas the IP₃ concentrations were elevated in the hippocampi of the ipsilateral and contralateral hemisphere and in the cortex of ipsilateral hemisphere at 5 min postinjury, no elevation in these sites was found at 20 min postinjury. Histologic analysis revealed neuronal damage in the cortex and CA3 regions of hippocampus ipsilateral to the injury at 24 h postinjury. The present results suggest activation of the phosphoinositide signal transduction pathway at the onset of injury and of a possible requirement of early persistent metabolic dysfunction (>20 min) such as the lactate accumulation in the delayed neuronal damage.     

Magnesium-deficiency potentiates free radical production associated with postischemic injury to rat hearts: Vitamin E affords protection

Preexisting magnesium deficiency may alter the susceptibility of rat hearts to postischemic oxidative injury (free radicals). This was examined in rats maintained for 3 weeks on a magnesium-deficient (Mg-D) diet with or without concurrent vitamin E treatment (1.2 mg/day, SC). Magnesium-sufficient (Mg-S) rats received the same diet supplemented with 100 mmol Mg/kg feed. Following sacrifice, isolated working hearts were subjected to 30-, 40-, or 60-min global ischemia and 30-min reperfusion. Postischemic production of free radicals was monitored using electron spin resonance (ESR) spectroscopy and spin trapping with -phenyl-N-tert butylnitrone (PBN, 3 mM final); preischemic and postischemic effluent samples were collected and then extracted with toluene. PBN/alkoxyl adduct(s) (PBN/RO·; _H = 1.93 G,_N = 13.63 G) were the dominant signals detected in untreated Mg-S and Mg-D postischemic hearts, with comparably higher signal intensities observed for the Mg-D group following any ischemic duration. Time courses of postischemic PBN/RO· detection were biphasic for both groups (maxima: 2–4 and 8.5–12.5 min), and linear relationships between the extent of PBN/RO· production and the severity of both mechanical dysfunction and tissue injury were determined. Following each duration of ischemia, Mg-D hearts displayed greater levels of total PBN adduct production (1.7 –2.0 times higher) and lower recovery of cardiac function (42–48% less) than Mg-S hearts. Pretreating Mg-D rats with vitamin E prior to imposing 40-min ischemia/reperfusion, led to a 49% reduction in total PBN/RO· production, a 55% lower LDH release and a 2.2-fold improvement in functional recovery, compared to untreated Mg-D hearts. These data suggest that magnesium deficiency predisposes postischemic hearts to enhanced oxidative injury and functional loss, and that antioxidants may offer significant protection against pro-oxidant influence(s) of magnesium deficiency.