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Fig. 3 | Particle and Fibre Toxicology

Fig. 3

From: Acute and subchronic exposure to air particulate matter induces expression of angiotensin and bradykinin-related genes in the lungs and heart: Angiotensin-II type-I receptor as a molecular target of particulate matter exposure

Fig. 3

Acute exposure to PM modifies [3H]-Angiotensin-II binding to the lung tissue membranes. a) Saturation binding. Membranes, obtained from naïve animals as described in Methods, were incubated with the indicated concentrations of [3H]-Angiotensin-II. Specific receptor binding was determined by subtracting the binding in the presence of 100 μM telmisartan from the total binding. The points show the means from quadruplicate determinations from a single experiment, which was repeated twice more with membranes obtained from different naïve animals. The line drawn is the best fit to a hyperbola. Best-fit values for the equilibrium dissociation constant (K d) and maximum binding (Bmax) are given in the text. b) Single-point determinations. Membranes were obtained from animals exposed to coarse (CP), fine (FP) and ultrafine particulate (UFP) or from the filtered air control group (FA), and then incubated with 10 nM [3H]-Angiotensin-II. Specific receptor binding was determined by subtracting the binding in the presence of 10 μM telmisartan. Scatter dot plot shows the value of the median. * Indicates significant differences among groups (n = 4 per group, p < 0.05)

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