@article{bentley_grubb_1991, title={EFFECTS OF A ZINC-DEFICIENT DIET ON TISSUE ZINC CONCENTRATIONS IN RABBITS}, volume={69}, ISSN={["0021-8812"]}, DOI={10.2527/1991.69124876x}, abstractNote={Young male New Zealand White rabbits given a diet containing 2 ppm of Zn (Zn-deficient diet) ceased to grow after 5 wk. Control rabbits given diets containing 80 or 85 of ppm Zn and experimental animals given 7 ppm of Zn (low-Zn diet) grew normally. The rabbits given the Zn-deficient diet also exhibited alopecia, skin lesions, and frequent pasteurella infections. These conditions were not observed in rabbits fed the other diets. The testes and thymus were smaller in the rabbits fed the Zn-deficient diet than in rabbits fed the control diet. Serum Zn concentrations in rabbits given the low- or Zn-deficient diets reached new lower levels after 2 wk, and these concentrations were maintained for up to 12 wk. The serum Zn concentration was, however, lower in the rabbits fed the Zn-deficient diet (approximately .35 micrograms/ml compared with .8 micrograms/ml for rabbits fed the low-Zn diet and 1.4 micrograms/ml for rabbits fed the control diet). Tissue Zn concentrations generally declined in rabbits fed the low- and Zn-deficient diets, but this response depended on the particular tissue and diet. Zinc levels in bone decreased by approximately 45% and in fur by 20 to 30% on either low-Zn or Zn-deficient treatments. With a Zn-deficient diet, Zn in liver and testes decreased by 20%, Zn in skin by 35%, and Zn in brain by 10%. The Zn concentration in the skeletal muscle and thymus was, however, maintained. In the eye, Zn concentration in the aqueous humor declined by approximately 20% in rabbits fed the Zn-deficient diet.(ABSTRACT TRUNCATED AT 250 WORDS)}, number={12}, journal={JOURNAL OF ANIMAL SCIENCE}, author={BENTLEY, PJ and GRUBB, BR}, year={1991}, month={Dec}, pages={4876–4882} }
 @article{mcgahan_matthews_bentley_1986, title={Effects of melittin on a model renal epithelium, the toad urinary bladder}, volume={855}, DOI={10.1016/0005-2736(86)90189-6}, abstractNote={The bee venom melittin, 10(-6) M, on the mucosal (urinary) side of the toad urinary bladder (in vitro), markedly decreased transepithelial potential difference, short-circuit current (Isc, sodium-dependent) and resistance. However, these effects were not seen when the toxin was placed on the opposite (serosal) side of the membrane preparation. The electrical effects were accompanied by a large increase in the transepithelial permeability to 22Na. The response was not changed by meclofenamic acid (which blocks formation of prostaglandins) but it was inhibited by La3+. In the presence of amiloride, which usually inhibits active Na transport and Isc, melittin, on the mucosal side, increased the Isc. The action of melittin appears to involve an interaction with anionic sites, which mediate its effects. Such sites appear to be present on the apical plasma membranes of the toad bladder epithelial cells, but they are not as abundant or they are inaccessible on the basal plasma membrane.}, journal={Biochimica et Biophysica Acta}, author={McGahan, M. C. and Matthews, D. O. and Bentley, P. J.}, year={1986}, pages={63–67} }
 @article{mcgahan_hazard_bentley_1985, title={Melittin-induced changes in Na and Cl movements across toad's skin and cornea (in vitro) of the toad, Bufo marinus}, DOI={10.1016/0742-8413(85)90165-3}, abstractNote={1. Melittin, from bee venom, increases short-circuit current (Isc) across the skin and cornea of toads. 2. In skin this reflects a rise in the influx of Na and is inhibited by meclofenamic acid (inhibits prostaglandin synthetase). 3. In corneas with melittin on the inside the rise in Isc is inhibited by bumetanide (inhibits Cl transport) and meclofenamic acid. 4. Melittin on the tear side of the cornea causes a biphasic change in Isc, and a rise in all undirectional fluxes of Na and Cl. 5. This effect was not changed by bumetanide or meclofenamic acid. 6. Melittin apparently has two types of effects, one mediated by prostaglandins while the other is more direct.}, journal={Comparative Biochemistry and Physiology}, author={McGahan, M. C. and Hazard, R. L. and Bentley, P. J.}, year={1985}, pages={291–296} }
 @article{mcgahan_chin_bentley_1983, title={CALCIUM-METABOLISM OF THE RABBIT LENS}, volume={36}, ISSN={["0014-4835"]}, DOI={10.1016/0014-4835(83)90089-1}, abstractNote={The Ca concentration in the rabbit lens is less than that in its bathing aqueous and vitreous humors. This Ca is not distributed evenly in the tissue; it has a higher concentration in the outer peripheral than the inner parts of the organ. About 60% of the total lenticular Ca is present in a layer extending about 0.5 mm down from the outer surface (25% of the total tissue in the lens). When incubated in a solution containing 45Ca about 40% of the lenticular Ca readily exchanges with the isotope in 3 hr; no further change occurred over the next 21 hr. This exchange appeared to occur across either the anterior or posterior side of the lens. The accumulated 45Ca was found to be present in a surface layer about 1 mm deep. The remaining 60% of the lenticular Ca was difficult to displace. Incubation for 5 hr in a Ca-free solution containing EDTA or following freezing and thawing resulted in a loss of only an additional 20% of tissue Ca. The remaining 'immobilizable' Ca (40%) was present in both the nuclear and peripheral zones of the lens. When the Ca concentration of the external medium is raised, lens Ca rises also, and when the external concentration is reduced the tissue level declines. In the presence of metabolic inhibitors (iodoacetate plus cyanide) lenticular Ca rises. This effect is slow; little change was seen in 5 hr. Ca accumulation in the lens was enhanced by the Ca ionophore A23187 but an effect was not detectable in 5 hr. Incubation in Na-free media or ouabain did not influence Ca accumulation suggesting that a Ca-Na exchange is not involved in regulation. Quercetin and orthovanadate, which can inhibit Ca-activated ATPase in some tissues were without effect on lens calcium. The phenothiazine trifluoperazine (TFP), however, enhanced accumulation of Ca. Efflux of accumulated 45Ca from the lens was rapid; 60% in 10 min and 90% in 3 hr. Lanthanum reduced the latter to 60% loss. Efflux of Ca from the lens was unchanged, under experimental conditions, by metabolic inhibitors, by EGTA, verapamil, TFP and vanadate.}, number={1}, journal={EXPERIMENTAL EYE RESEARCH}, author={MCGAHAN, MC and CHIN, B and BENTLEY, PJ}, year={1983}, pages={57–66} }
 @article{mcgahan_chin_bentley_1983, title={SOME OBSERVATIONS ON THE MAGNESIUM-METABOLISM OF THE RABBIT LENS}, volume={36}, ISSN={["0014-4835"]}, DOI={10.1016/0014-4835(83)90090-8}, abstractNote={The (Mg) concentration in the rabbit lens is about 3.25 mmol/kg wet wt or 4.7 mM. This level is much greater than that in the bathing aqueous and vitreous humors. The Mg concentration in the peripheral part of this tissue is about four times greater than that in the inner 'nuclear' regions. Exchanges of Mg between the lens and its bathing fluids are very slow; under control conditions the lens appears to be virtually impermeable to Mg. Exposure to metabolic inhibitors, depolarizing concentrations of potassium, ouabain or replacement of Na with Li had little effect on the Mg content of the lens. Incubation of lenses in solutions containing EDTA or following freezing and thawing suggested that much of the Mg is present in a bound form. The ionophore A-23187 increased the permeability of the lens to Mg. Adjustment of the external Mg level in the presence of A-23187 indicated that the internal 'free' Mg concentration was about 3 mM. This result suggests that about 35% of the lenticular magnesium is bound.}, number={1}, journal={EXPERIMENTAL EYE RESEARCH}, author={MCGAHAN, MC and CHIN, B and BENTLEY, PJ}, year={1983}, pages={67–73} }
 @article{bentley_mcgahan_1982, title={A PHARMACOLOGICAL ANALYSIS OF CHLORIDE TRANSPORT ACROSS THE AMPHIBIAN CORNEA}, volume={325}, ISSN={["0022-3751"]}, DOI={10.1113/jphysiol.1982.sp014163}, abstractNote={1. Active Cl, but not Na, transport across the toad cornea was inhibited by mepacrine, which is a phospholipase A2 inhibitor; trifluoperazine, which blocks the action of calmodulin; and meclofenamic acid, which inhibits synthesis of prostaglandins. Bumetanide and DIDS (4,4'‐diisothiocyano‐2,2'‐stilbene disulphonic acid) have previously been shown to inhibit this Cl transport. The interactions of these antagonists with several agonists that increase Cl transport were studied. 2. The effects of adrenaline, prostaglandin E2, dibutyryl cyclic AMP (DBcAMP) and the Ca ionophore A23187 were inhibited by mepacrine, trifluoperazine and bumetanide. 3. The inhibitory effects of high concentrations of DIDS, however, could be overcome by all of the agonists except DBcAMP. 4. Meclofenamic acid only blocked the effects of A23187. 5. A model is proposed to account for the observed actions and interactions of the various antagonists and agonists on Cl transport. This involves possible roles for Ca, calmodulin and phospholipase A2.}, number={APR}, journal={JOURNAL OF PHYSIOLOGY-LONDON}, author={BENTLEY, PJ and MCGAHAN, MC}, year={1982}, pages={481–492} }
 @article{mcgahan_bentley_1982, title={STIMULATION OF TRANS-EPITHELIAL SODIUM AND CHLORIDE TRANSPORT BY ASCORBIC-ACID - INDUCTION OF NA+ CHANNELS IS INHIBITED BY AMILORIDE}, volume={689}, ISSN={["0006-3002"]}, DOI={10.1016/0005-2736(82)90273-5}, abstractNote={Ascorbic acid increases the short circuit current (Isc) across the amphibian cornea when it is present at either surface of this epithelium. These effects were additive. The effect was greater when it was on the tear side. The response returned to baseline levels when the ascorbic acid was washed from the bathing media. The effect of ascorbic acid on Isc when it was on the aqueous humor side of the cornea could be blocked by bumetanide but that due to the vitamin's presence on the tear side was unchanged. The ascorbic acid could enter the tissue and crossed the cornea at similar rates in either direction. When the cornea was bathed by a Cl−-free solution or exposed to bumetanide, the rise in Isc observed with ascorbic acid on the tear side was equivalent to an increased Na+ flux from the tear to the aqueous humor side. In normal (Cl− present) Conway solution the rise in the Isc seen with ascorbic acid on the aqueous humor side was equal to an increased flux of Cl− from the aqueous to the tear surface. However, when ascorbic acid was present on the opposite, tear, side the increased Isc reflected a rise in both Cl− and Na+ transport, aqueous-to-tear side, and tear-to-aqueous side, respectively. Thiol reagents (tear side), including reduced glutathione (10−5 M), blocked the effect of ascorbic acid (10−3 M) providing they were added to the bathing solution prior to the vitamin. However, they had no effect once the response had been established. The effect of the reduced glutathione appeared to be of a non-competitive nature. Oxidized glutatione (10−4 M) (and cystamine) blocked the effect of ascorbic acid (10−3 M) when present on the tear side prior to the vitamin. However, they also increased the rate of decline of the response when added subsequently to the ascorbic acid. Amiloride (as low as 5·10−9 M), on the tear side but not the aqueous humor side, prevented the response to ascorbic acid but could not reverse it, once it was established. The possible nature of the effect of ascorbic acid is discussed in relation to its pharmacological interactions with thiol and disulfide reagents and amiloride.}, number={2}, journal={BIOCHIMICA ET BIOPHYSICA ACTA}, author={MCGAHAN, MC and BENTLEY, PJ}, year={1982}, pages={385–392} }
 @article{mcgahan_bentley_1981, title={Alpha-aminoisobutyric acid transport in the amphibian crystalline lens}, volume={34}, journal={Journal of Physiology (London)}, author={McGahan, M. C. and Bentley, P. J.}, year={1981}, pages={49–56} }
 @article{mcgahan_bentley_1981, title={INHIBITION OF ALPHA-AMINOISOBUTYRIC-ACID UPTAKE BY DIISOTHIOCYANOSTILBENEDISULPHONIC ACID IN THE AMPHIBIAN CORNEA}, volume={643}, ISSN={["0006-3002"]}, DOI={10.1016/0005-2736(81)90240-6}, abstractNote={α-Aminoisobutyric acid accumulation of the toad's (Bufo marinus) cornea and lens is inhibited by 4,4′-diisothiocyano-2,2′-stilbenedisulfonic acid. This effect is seen at pH 8.4; at pH 7.4 a small increase in aminoisobutyric acid uptake was observed. Efflux of aminoisobutyric acid is unchanged by diisothiocyanostilbenedisulphonic acid at either pH. The inhibitory effect of diisothiocyanostilbenedisulphonic acid on aminoisobutyric acid accumulation appears to reflect a direct action on membrane mechanisms that mediate its influx.}, number={1}, journal={BIOCHIMICA ET BIOPHYSICA ACTA}, author={MCGAHAN, MC and BENTLEY, PJ}, year={1981}, pages={261–264} }
 @article{bentley_mcgahan_1980, title={INHIBITORY-ACTION OF DIDS ON CHLORIDE TRANSPORT ACROSS THE AMPHIBIAN CORNEA}, volume={304}, ISSN={["0022-3751"]}, DOI={10.1113/jphysiol.1980.sp013340}, abstractNote={1. DIDS (4,4'‐diisothiocyano‐2,2'‐stilbene disulphonic acid) reduced the CI Isc across the toad's (Bufo marinus) cornea. It acted on either the aqueous or tear side and these effects were additive. 2. The reduction in the Isc was equivalent to the decline in the undirectional flux of Cl from the aqueous to the tear side. The Cl flux from tear to aqueous was not changed. 3. DIDS did not change transmural Na transport. 4. The action of the diuretic bumetanide, which also inhibits Cl transport was additive to that of DIDS when both compounds were present on the aqueous though not when they were on the tear side of the cornea. 5. The results are consistent with the role of a Cl‐/anion exchange mechanism in active Cl transport across the cornea. 6. A hypothesis regarding the interactions and site of action of bumetanide in relation to that of DIDS, and the Cl transport process, is proposed.}, number={JUL}, journal={JOURNAL OF PHYSIOLOGY-LONDON}, author={BENTLEY, PJ and MCGAHAN, MC}, year={1980}, pages={519–527} }
 @article{mcgahan_yorio_bentley_1977, title={The mode of action of bumetanide: inhibition of chloride transport across the amphibian cornea}, volume={203}, journal={Journal of Pharmacology and Experimental Therapeutics}, author={McGahan, M. C. and Yorio, T. and Bentley, P. J.}, year={1977}, pages={97–102} }