GROWTH DELAY INDUCED IN <i>ESCHERICHIA COLI</i> BY NEAR‐ULTRAVIOLET RADIATION: RELATIONSHIP TO MEMBRANE TRANSPORT FUNCTIONS*

Kubitschek, H.E.; Doyle, Ronald J.

doi:10.1111/j.1751-1097.1981.tb05476.x

Cited by 19 publications

(9 citation statements)

References 14 publications

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“…Numerous studies demonstrate a remarkably similar photoinduced growth delay caused by near-UV light in laboratory studies on pure cultures of Eschenchia coli and other bacteria (Jagger et al 1964, Eisenstark 1971, Ramabhadran & Jagger 1975, Kubitschek & Doyle 1981. In these studies, as in the present study (Fig.…”

Section: Discussionsupporting

confidence: 76%

Sunlight-induced growth delay of planktonic marine bacteria in filtered seawater

Sieracki¹,

Sieburth²

1986

Mar. Ecol. Prog. Ser.

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The growth of natural populations of planktonic manne bacter~a was observed upon exposure to natural sunhght In Narragansett Bay seawater with most of the phototrophic and bactenagrazing nanoflagellates removed by filtrabon, a shght increase in bactenal populahons began after 24 to 36 h in the dark In populabons exposed to sunlight, growth was delayed further Dilutmg the bactena-dom~nated size frachon (< 0 6 pm) with 0 2 pm filtered seawater resulted in a shorter lag penod and more rapid growth than unrllluted filtrates Sunlight caused a s~g n~f~c a n t lengthening of the lag penod but did not affect the exponenbal growth rate suggesbng that the bacteria were susceptible to sunhght whlle undergo~ng protein synthesis pnor to euponenhal growth Use of spectral fllters indicated that the growth delay was pnmanly due to UV-A wavelengths (320 to 400 nm) These results are analogous to sunl~ght effects on bacteria observed in pure culture experiments Use of neutral density fdters ~ndicated that the effect was pronounced at 50 and 25"L of surface sunlight and detectable at 16 O/O Photo~nhib~tion of bactenal activities could be a signif~cant factor in the d~e l cychng of organic matter nutr~ents and reactlve gases m the euphot~c zone of the oceans

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Section: Discussionsupporting

confidence: 76%

Sunlight-induced growth delay of planktonic marine bacteria in filtered seawater

Sieracki¹,

Sieburth²

1986

Mar. Ecol. Prog. Ser.

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“…It could also be true in cells in which repair of DNA damage is efficient. Kubitschek and Doyle (1981) and Moss and Smith (1981) have suggested that membrane damage is significant in the killing of E, coli by UV-A. Sarachek and Higgins (1972) have made similar proposals with regard to Candida albicans exposed to UV-C radiation.…”

Section: Physiological Significance Of Uv Effects On Membranesmentioning

confidence: 87%

Membranes as targets of ultraviolet radiation

Murphy

1983

Physiologia Plantarum

126

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In non‐photosynthetic cells, evidence for UV (ultraviolet radiation) damage to membranes comes from electron microscopy, chemical analysis and observations of transport processes. Specific perturbations in transport across membranes occur quickly after a relatively low fluence of UV. As an example, irradiation of suspension‐cultured rose cells with 500‐2000 J m−2 (at 254 nm) causes an appearance of K+ in the extracellular medium at the rate of 5 × 10−10μmol cell−1 min−1 for 30 to 60 min and more slowly thereafter. The early, rapid phase of appearance of K+ reflects both an increase in efflux and a decrease in influx. The appearance of K+ is matched by an appearance of HCO−3 in the medium. The HCO−3 comes from respiratory CO2, which hydrates and dissociates in the cytoplasm, leading to a decrease in cytoplasmic pH. Overall, these results not only demonstrate UV damage to membrane function, but also suggest several ways by which UV may alter the general metabolic state of the cell. A demonstration of direct effects of UV on membrane components requires a purified system. At lower fluence, < 1800 J m−2 (254 nm), the ATPase of membrane vesicle preparations is inactivated in a two‐phase process that suggests the presence of enzymes with different UV sensitivities. The existence of two non‐mitochondrial enzymes in rose cell vesicles has been confirmed by solubilizing the vesicle proteins with 1% cholic acid and separating the components on G‐150 Sephadex. One component of relatively high molecular weight is especially sensitive. The fact that it is still sensitive when it is dissolved in cholic acid strongly suggests that its sensitivity is intrinsic and does not depend on sensitization by other membrane components. The action spectrum for the inactivation of the ATPase has a major peak at 290 nm and extends into the UV‐C and UV‐A regions. The physiological effects of UV‐stimulated membrane changes are uncertain. There is little evidence that the UV damage to membranes is responsible for cell death. A UV‐induced loss of K+ from guard cells may result in lower stomatal conductance. UV‐stimulated membrane changes may play a role in the UV‐induced synthesis of anthocyanins.

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“…These lead to the production of peroxides, considered to be primary damaging agents (Kramer andAmes 1987, Leven et al 1990) . Highly detrimental to cell membrane structure and function, peroxidation has been linked to increased ion permeability Smith 1981, Kelland et al 1984), fluidity loss (Quin 1981) and inactivation of membrane enzymes (Kubitschek and Doyle 1981, Sharma and Jagger 1981, Pizarro and Orce 1988 . The subject has been reviewed, from a purely photochemical/photobiological perspective (Girotti 1990) .…”

Section: Discussionmentioning

confidence: 97%

“…Others have reported a close relationship between membrane damage and the UV-A-induced growth delay (Koch et al 1976, Taber et al 1978, Kubitschek and Doyle 1981 . In a previous paper the occurrence of membrane perturbations, induced in E .…”

Section: Introductionmentioning

confidence: 96%

UV-A Oxidative Damage Modified by Environmental Conditions inEscherichia Coli

Pizarro

1995

International Journal of Radiation Biology

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The effect of sublethal fluences (50-200 kJ m-2) of UV-A radiation (320-400 nm) in bacterial cells is a transient growth inhibition related to photo-modified tRNA and is associated with changes in membrane structure and function. Higher UV-A fluences result in cell death due to the production of reactive oxygen species, so far undetected at sublethal doses. Oxidative mechanisms of toxicity induced by 120 kJ m-2 UV-A radiation can be recorded by ultra-weak chemiluminescence, useful in quantifying oxidative reactions. When Escherichia coli was exposed to UV-A stress at a fluence rate equivalent to that of the Sun in the biosphere (33 W m-2), chemiluminescence levels were proportional to the photodamage. Chemiluminescence and photo-damage are linearly proportional and dependent on environmental conditions of the cells. It is postulated that in addition to tRNA photo-modification, UV-A alters the membrane structure of E. coli by oxidative damage, since changes in the membrane structure under different environmental conditions play a key role in the cell's response to UV-A injury.

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GROWTH DELAY INDUCED IN ESCHERICHIA COLI BY NEAR‐ULTRAVIOLET RADIATION: RELATIONSHIP TO MEMBRANE TRANSPORT FUNCTIONS*

Cited by 19 publications

References 14 publications

Sunlight-induced growth delay of planktonic marine bacteria in filtered seawater

Sunlight-induced growth delay of planktonic marine bacteria in filtered seawater

Membranes as targets of ultraviolet radiation

UV-A Oxidative Damage Modified by Environmental Conditions inEscherichia Coli

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