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G N Johnson

Publications and source records attributed to G N Johnson.

6 recordsLinked to original sources

In vivo temperature dependence of cyclic and pseudocyclic electron transport in barley.

The effect of temperature on the rate of electron transfer through photosystems I and II (PSI and PSII) was investigated in leaves of barley (Hordeum vulgare L.). Measurements of PSI and PSII photochemistry were made in 21% O2 and in 2% O2, to limit electron transport to O2 in the Mehler reaction. Measurements were made in the presence of saturating CO2 concentrations to suppress photorespiration. It was observed that the O2 dependency of PSII electron transport is highly temperature dependent. At 10 degrees C, the quantum yield of PSII (phi PSII) was insensitive to O2 concentration, indicating that there was no Mehler reaction operating. At high temperatures (> 25 degrees C) a substantial reduction in phi PSII was observed when the O2 concentration was reduced. However, under the same conditions, there was no effect of O2 concentration on the delta pH-dependent process of non-photochemical quenching. The rate of electron transport through PSI was also found to be independent of O2 concentration across the temperature range. We conclude that the Mehler reaction is not important in maintaining a thylakoid proton gradient that is capable of controlling PSII activity, and present evidence that cyclic electron transport around PSI acts to maintain membrane energisation at low temperature.

Biological Transport, Active↗

Inhibition of electron transport at the cytochrome b(6)f complex protects photosystem II from photoinhibition.

Photoinhibition of photosystem II (PS II) activity was studied in thylakoid membranes illuminated in the presence of the inhibitor of the cytochrome b(6)f complex 2'iodo-6-isopropyl-3-methyl-2',4, 4'-trinitrodiphenylether (DNP-INT). DNP-INT was found to decrease photoinhibition. In the absence of DNP-INT, anaerobosis, superoxide dismutase and catalase protected against photoinhibition. No effect of these treatments was observed in the presence of DNP-INT. These data demonstrate that photoinhibition under these conditions is caused by reactive oxygen species which are formed most probably by the reduction of oxygen at photosystem I. The results are discussed in terms of the importance of photosynthetic control in protection against photoinhibition in vivo.

Anaerobiosis↗

Chlorophyll fluorescence--a practical guide.

Chlorophyll fluorescence analysis has become one of the most powerful and widely used techniques available to plant physiologists and ecophysiologists. This review aims to provide an introduction for the novice into the methodology and applications of chlorophyll fluorescence. After a brief introduction into the theoretical background of the technique, the methodology and some of the technical pitfalls that can be encountered are explained. A selection of examples is then used to illustrate the types of information that fluorescence can provide.

Chlorophyll↗

Maternal halothane anesthesis reduces cerebral blood flow in the acidotic sheep fetus.

Cerebrovascular autoregulation is lost during fetal asphyxia as cerebral vessels undergo compensatory vasodilation. In such a situation, maternal anesthetics, which decrease fetal arterial blood pressure and cardiac output, may further aggravate cerebral hypoxia. To examine this possibility, we prepared six pregnant ewes in such a manner as to be able to measure fetal regional cerebral blood flow in utero during acidosis produced by partial umbilical cord compression both before and after 15 minutes of halothane anesthesia given to the mother. Umbilical cord compression in the absence of anesthesia caused fetal metabolic and respiratory acidosis as evidenced by a decrease in arterial pH from 7.34 to 7.05; fetal arterial oxygen saturation simultaneously decreased from 29 to 17%. Halothane anesthesia administered to the mother of the acidotic fetus caused further aggravation of fetal acidosis (arterial pH 6.85) and oxygen desaturation (10%) and the fetus became markedly hypotensive. Blood flow to four cerebral areas increased 27 to 69% above control levels in the fetus during acidosis in the absence of maternal anesthesia but decreased to levels 30 to 42% below acidosis values when maternal anesthesia was combined with fetal acidosis. These data suggest that potent cardiovascular depressant anesthetics administered to the mother in the presence of fetal acidosis could decrease fetal cerebral oxygen delivery by interfering with fetal cardiovascular compensation during acidosis and reducing fetal cerebral blood flow.

Acid-Base Equilibrium↗

Regional cerebral blood flow changes during severe fetal asphyxia produced by slow partial umbilical cord compression.

We studied the effects of severe partial asphyxia on regional cerebral blood flow and arterial blood pressure in the unanesthetized, physiologically stable fetal lamb. Cerebral blood flow was measured by the microsphere technique before and during partial umbilical cord compression. Asphyxia sufficient to decrease pH from 7.40 to 7.04 and reduce oxygen saturation from 50% to 19% increased cerebral blood flow to all areas of the brain with the largest increases going to the brain stem (275% of control) and deep cerebral structures (240% of control). Fetal arterial blood pressures increased from a mean of 58 mm Hg to a mean of 71 mm. Hg during asphyxia. The blood pressure increases correlated closely with the regional cerebral blood flow increases. There was a poor correlation between cerebral blood flow increases and changes in Paco2' pH, or oxygen saturation. We conclude that during severe fetal asphyxia arterial blood pressure is the critical factor in determining cerebral blood flow.

Acidosis↗