The structural mimicry of membrane sterols by tamoxifen: evidence from cholesterol coefficients and molecular-modelling for its action as a membrane anti-oxidant and an anti-cancer agent

The anti-cancer drug tamoxifen is a potent inhibitor of lipid peroxidation induced by Fe(III)-ascorbate in ox-brain phospholipid liposomes. Similar anti-oxidant effects, but with varying potencies, are also shown by 4-hydroxytamoxifen, cholesterol, ergosterol and 17-β-oestradiol. We now describe a computer-graphic fitting technique that demonstrates a structural similarity between the five compounds. In addition, we have quantified the differences (relative to cholesterol) between the anti-oxidant activities of the compounds in terms of a novel expression reffered to here as the cholesterol coefficient (C_c) Finally, we discuss how the inhibitory effect of tamoxifen on lipid peroxidation may result from a membrane stabilization that is associated with a decrease in membrane fluidity. This action may be related to the anti-proliferative effect exerted by tamoxifen on cancer and fungal cells.     

Studies on hemolysis of human erythrocytes by linoleic acid

The results presented in this paper show that lysis of human erythrocytes by linoleic acid is not caused by peroxidation of the fatty acid. Peroxidase, superoxide dismutase and scavengers of O ₂ ⁻ and OH had no effect on the lysis while catalase showed only marginal inhibition suggesting that O ₂ ⁻ , OH, O ₂ ⁻ and H₂O₂ do not play any direct role in hemolysis by linoleic acid. Generators of H₂O₂ inhibited the lysis completely and methemoglobin cells were more resistant to hemolysis by linoleic acid. The fatty acid did neither bind to nor fomed complex with red cell ghosts. Membrane oxidation of sulphydryl groups was also not involved in the lysis. Β-Carotene, retinol and bile salts enhanced the lysis, while, cholesterol but not cholesterol acetate, inhibited it. Taurocholate-pretreated cells were more susceptible to linoleic acid lysis. These observations suggested-that lysis by linoleic acid may be due to its detergent property.     

Dealing with detection error in site occupancy surveys: what can we do with a single survey?

Aim Site occupancy probabilities of target species are commonly used in various ecological studies, e.g. to monitor current status and trends in biodiversity. Detection error introduces bias in the estimators of site occupancy. Existing methods for estimating occupancy probability in the presence of detection error use replicate surveys. These methods assume population closure, i.e. the site occupancy status remains constant across surveys, and independence between surveys. We present an approach for estimating site occupancy probability in the presence of detection error that requires only a single survey and does not require assumption of population closure or independence. In place of the closure assumption, this method requires covariates that affect detection and occupancy.Methods Penalized maximum-likelihood method was used to estimate the parameters. Estimability of the parameters was checked using data cloning. Parametric boostrapping method was used for computing confidence intervals.Important findings The single-survey approach facilitates analysis of historical datasets where replicate surveys are unavailable, situations where replicate surveys are expensive to conduct and when the assumptions of closure or independence are not met. This method saves significant amounts of time, energy and money in ecological surveys without sacrificing statistical validity. Further, we show that occupancy and habitat suitability are not synonymous and suggest a method to estimate habitat suitability using single-survey data.     

Heavy-metal toxicity in the cyanobacterium Nostoc Linckia

The effects of HgCl₂, NiCl₂ and CoCl₂ on Nostoc linckia (Roth) Born. et Flah. were studied. Low level (0.2 p.p.m.) of mercury increased heterocyst frequency, stimulated nitrate reductase and ammonium uptake, but significantly inhibited acetylene-reducing and glutamine-synthetase activities. In contrast, NiCl₂ and CoCl₂ greatly inhibited all of the above processes.