Inhibition of conversion of geranylgeranyl-chlorophyll to phytol-chlorophyll by S-ethyl dipropylthiocarbamate (EPTC)

The influence of EPTC (S-ethyl dipropylthiocarbamate) on the hydrogenation of geranylgeranylchlorophyll (GG-Chl) to phytol-Chl was studied during the greening (6-, 12-, 18-, 24-, and 48-hr incandescent light exposure) of etiolated wheat [Triticum aestivum (L.) cv “Stacy”] and sorghum [Sorghum bicolor (L.) Moench cv “G 522DR”] seedlings grown in nutrient solution containing ¹⁴C-labeled sodium acetate. Chloroplast pigment synthesis occurred and small quantities of GG-Chl were found in both Chl^?a and Chl^?b. When wheat seedlings were greened for 48 hr in an EPTC concentration series (1 nM to 100 μM), geranylgeraniol (GG) content increased from 11% (control) to 60% (100 μM EPTC) of the isoprenoid alcohol esterified to chlorophyllide a, but Chl-b contained ≤1% GG-Chl at all concentrations of EPTC. Sorghum seedlings greened for 48 hr in the same EPTC concentration series contained about 3% GG (control) while 100 and 40% GG esterified to chlorophyllide a and chlorophyllide b, respectively, after 48 hr exposure to 100 μM EPTC. Thus, EPTC prevented hydrogenation of GG-Chl to phytol-Chl on the Chl molecule more in sorghum than in wheat.     

Locomotion and chemotaxis of mononuclear phagocytes

The capacity for locomotion and for chemotaxis is probably very different in monocytes and macrophages from different sources. Numerous techniques have been established for studying the locomotion of these cells. Many of the factors are sparsely documented and the reports are scattered among various cell types. Heterogeneity of locomotion and chemotactic responsiveness is evident when established macrophage lines and mouse peritoneal macrophage are studied. The effects of mononuclear phagocytes and their released products on the locomotion of other cell types are reviewed.     

Black soil blindness: A new mycotoxicosis of cattle grazing Corallocytostroma-infected Mitchell grass (Astrebla spp)

A new, fatal mycotoxicosis of cattle has been recognised in north-western Australia. A feeding trial confirmed the toxicity of a previously unknown species of Corallocytostroma that grows on Mitchell grass (Astrebla spp). The disease has been colloquially named ‘black soil blindness’ because its most prominent features are its confinement to pastures on black soil, and blindness and death of affected animals. Over 500 cattle have died and considerable subclinical disease is present. Above average wet season rainfall and extended growing seasons may explain the emergence of the fungus. The disease is important because cattle production in large areas of Australia utilise Mitchell grass pastures.     

Gibberellin influence on membrane disruption by thiocarbamate herbicides

Vernolate (0, 8, 16, 31, 62, 125.0, or 250.0 ppbw) incorporated into sand inhibited the growth of wheat (Triticum aestivum L. cv Holley) at 125.0 ppbw. These growth inhibition and morphological responses were virtually identical to wheat response to EPTC at 125 ppbw. ¹⁴C from vernolate (carbonyl labeled) (125.0 ppbw) was absorbed into wheat seedlings at approximately 1.8 μM on the presumption that the ¹⁴C present was [¹⁴C]vernolate. Since the response of wheat to the thiocarbamate herbicides resembles a gibberellic acid (GA) deficiency and cell enlargement requires the presence of functional plasmalemmas and tonoplasts, the question of membrane disruption by excessive concentrations of thiocarbamate herbicides and potential reversal thereof by GA₃ was studied by measuring the efflux of K⁺, Na⁺, and Mg²⁺. GA₃ (0.003 μM) stimulated lettuce leaf disc growth in diameter and fresh weight. This GA-stimulated increase in size and weight was reversed by 1 mM EPTC. Betacyanin efflux from beet leaf tonoplasts was increased by 1 mM EPTC and this efflux was not reversed by exogenous GA₃ (0.3 μM). This influence by supraoptimal EPTC concentrations was shown to be via membrane disruption, which obviated any possible GA influence by eliminating the functionality of the membranes requisite to the development of a GA response. It is concluded that viable mode-of-action studies must measure physiological responses consistent with the symptomology of herbicide responses normally observed with each herbicide at field concentrations.     

The pathogenic role of pulmonary intravascular macrophages in acute African swine fever

Recent studies of pulmonary intravascular macrophages have led to the re-examination of the mechanisms giving rise to alveolar oedema. A highly virulent isolate of African swine fever virus was replicated in pulmonary intravascular macrophages, interstitial and alveolar macrophages, fibroblasts and neutrophils. The alveolar oedema — characteristic of acute forms of African swine fever — and the vascular changes observed, which consisted of the formation of fibrin microthrombi in septal capillaries and the vacuolisation of endothelial cells, may have been due, however, to the activation of pulmonary intravascular macrophages, and not to the cytopathic effect subsequent to the replication of the African swine fever virus. Furthermore, it was observed that virus replication in cells not belonging to the mononuclear phagocyte system — such as fibroblasts and neutrophils — occurred earlier than in cells belonging to that system.     

Vascular leakage induced by histamine, bradykinin, serotonin and prostaglandin E2 in Greyhounds

SUMMARY Vascular leakage induced by intradermal injection of histamine, bradykinin and serotonin alone and co-injected with prostaglandin E₂ was measured in Greyhounds using ¹²⁵Iodine-labelled human serum albumin (¹²⁵I-HSA) as a marker in the blood. Histamine and bradykinin produced dose-dependent vascular leakage. At equimolar concentrations, histamine was more than twice as potent as bradykinin. Serotonin did not induce vascular leakage and was irritant. Prostaglandin E₂ did not induce significant vascular leakage (maximum 5μL) when injected alone, but when co-injected with histamine and bradykinin, the vascular leakage of both histamine and bradykinin was increased. This effect was more pronounced if lower concentrations of histamine and bradykinin were injected. The induced vascular leakage was greatest during the first five minutes of lesion development for histamine, during the second five minutes of lesion development for bradykinin, and the synergistic effect of prostaglandin E₂ was maximal during the third five minute period of lesion development.