The hydrogen sulfide donor, Lawesson's reagent, prevents alendronate-induced gastric damage in rats

Our objective was to investigate the protective effect of Lawesson's reagent, an H2S donor, against alendronate (ALD)-induced gastric damage in rats. Rats were pretreated with saline or Lawesson's reagent (3, 9, or 27 µmol/kg, po) once daily for 4 days. After 30 min, gastric damage was induced by ALD (30 mg/kg) administration by gavage. On the last day of treatment, the animals were killed 4 h after ALD administration. Gastric lesions were measured using a computer planimetry program, and gastric corpus pieces were assayed for malondialdehyde (MDA), glutathione (GSH), proinflammatory cytokines [tumor necrosis factor (TNF)-α and interleukin (IL)-1β], and myeloperoxidase (MPO). Other groups were pretreated with glibenclamide (5 mg/kg, ip) or with glibenclamide (5 mg/kg, ip)+diazoxide (3 mg/kg, ip). After 1 h, 27 µmol/kg Lawesson's reagent was administered. After 30 min, 30 mg/kg ALD was administered. ALD caused gastric damage (63.35±9.8 mm2); increased levels of TNF-α, IL-1β, and MDA (2311±302.3 pg/mL, 901.9±106.2 pg/mL, 121.1±4.3 nmol/g, respectively); increased MPO activity (26.1±3.8 U/mg); and reduced GSH levels (180.3±21.9 µg/g). ALD also increased cystathionine-γ-lyase immunoreactivity in the gastric mucosa. Pretreatment with Lawesson's reagent (27 µmol/kg) attenuated ALD-mediated gastric damage (15.77±5.3 mm2); reduced TNF-α, IL-1β, and MDA formation (1502±150.2 pg/mL, 632.3±43.4 pg/mL, 78.4±7.6 nmol/g, respectively); lowered MPO activity (11.7±2.8 U/mg); and increased the level of GSH in the gastric tissue (397.9±40.2 µg/g). Glibenclamide alone reversed the gastric protective effect of Lawesson's reagent. However, glibenclamide plus diazoxide did not alter the effects of Lawesson's reagent. Our results suggest that Lawesson's reagent plays a protective role against ALD-induced gastric damage through mechanisms that depend at least in part on activation of ATP-sensitive potassium (KATP) channels.

Efficacy of pirimiphos-methyl (50% EC), as a larvicide for the control of Culex quinquefasciatus.

Background & objectives: Pirimiphos-methyl, an organophosphorus insecticide is known to overcome resistance mechanisms of mosquitoes to other organophosphates. Information on the duration of efficacy of pirimiphos-methyl (50% emulsifiable concentrate) for the control of immatures of Culex quinquefasciatus, the vector of bancroftian filariasis, is scanty and hence site specific field trials are necessary to determine the field dosage. Pirimiphos-methyl (50% EC) was tested for its efficacy in cesspits and drains against the immatures of Cx. quinquefasciatus at Puducherry, an endemic area for filariasis, south India. Methods: In cesspits, Pirimiphos-methyl (50% EC) was tested at the dosage of 25, 50, 100 and 200 g(ai)/ ha and in drains at 50, 100 and 200 g(ai)/ha. Immature density during pre-treatment and post-treatment periods was recorded and the efficacy was determined by calculating percentage reduction in larval and pupal densities for a period of about one month. Results: In cesspits, application of the insecticide at 25 and 50 g(ai)/ha reduced the density of larvae by >80 per cent for 2-4 days only, whereas at 100 and 200 g(ai)/ha, the efficacy lasted for 7-8 days. More than 80 per cent reduction was observed in pupal density for 4 days at 50 g(ai)/ha and for 10-12 days at 100 and 200 g(ai)/ha respectively. In drains treated with 50 g (ai)/ha, >80 per cent reduction in larval density was recorded up to 3rd day post-treatment. The efficacy showing >80 per cent reduction in larval density lasted for 12-13 days and the same in pupal density lasted for 10-12 days at 100 and 200 g(ai)/ha. Interpretation & conclusions: At the dosages of 100 and 200 g(ai)/ha, pirimiphos-methyl (50% EC) showed no difference in the control of larvae of Cx. quinquefasciatus in cesspits and drains. Pirimiphosmethyl may be applied at the field dosage of 100 g (ai)/ha at 10 day-intervals in the larval habitats of Cx. quinquefasciatus to achieve >80 per cent reduction in immature density.

Influence of hexaconazole, carbofuran and ethion on soil microflora and dehydrogenase activities in soil and intact cell.

Total microbial count was highly affected (up to 61% at 1000 micrograms level) in presence of hexaconazole and persisted up to 21 days. Bacteria were more susceptible than actinomycetes. Carbofuran and ethion were moderately toxic to soil microflora. Inhibitory effects of all the three pesticides gradually decreased after 21 days as was evident by increase in total microbial count except in carbofuran. GDH activity in soil was also affected initially (up to 14 days) by all the three pesticides (60.3% in hexaconazole at 1000 micrograms level) and inhibition gradually decreased to zero except in carbofuran (15-20% toxicity persisted up to 35 days). GDH and LDH activity in presence of hexaconazole was strongly affected in intact cells of some standard culture of bacteria like Rhizobium sp. (host Dolichos sp., 32.1 and 72.5%), Bacillus subtilis Cohn (86.75 and 76.5%), Azotobacter sp. (36.9 and 55.4%) and B. sphaericus (67.6% GDH) respectively. Carbofuran inhibited the enzyme activity in B. subtilis (55.55 and 35.3%) and to some extent in B. sphaericus. Ethion moderately inhibited LDH activity in Rhodococcus sp. AK1 (17.1 and 33.3%), Rhizobium (27.6% LDH), E. coli HB 101 (34.2% LDH) as evidenced by formazan formation. From the result, it might be concluded that among the above three pesticides tested hexaconazole strongly inhibited the dehydrogenase system in bacteria including nitrogen fixing bacteria of soil and thus may affect soil fertility. It was concluded that hexaconazole was more toxic than ethion to dehydrogenase enzymes.

Identification and characterization of some PR-proteins induced by kitazin and Rhizoctonia solani causing sheath blight of rice.

Significant reduction (68.38%) in sheath blight disease of rice was noticed when foliar spray of a systemic fungicide, kitazin (480 micrograms mg-1), was applied twice at an interval of 2 days before inoculation. SDS-PAGE analysis of proteins of Rhizoctonia-infected rice leaf sheaths revealed the presence of 16 proteins ranging from 20 to 90 kDa (approx.). Six were identified as constitutive defense proteins (increased after infection), 6 as secondary defense proteins (formed de novo) and the rest 4 appeared non-defense proteins. Non-inoculated kitazin-treated leaf sheaths showed 15 proteins of which 5 were constitutive and 4 secondary defense proteins (both are PR-proteins). Among the PR-proteins, five beta-1,3-glucanases and one chitinase was identified and characterized. One rice chitinase (MW 20 kDa) and 2 glucanases (60 & 69 kDa) showed serological relationships with tobacco chitinase (32 kDa) and tobacco glucanase (33 kDa) respectively. The implications of results have been discussed in relation to biotic and abiotic induction of PR-proteins in rice.

Effect of defoliant (butiphose) on morpho-physiological properties and enzyme systems of natural membranes.

Butiphose (Tributyltritiophosphate, (C4H9S)3PO) a commonly used defoliant in cotton growing regions of USSR, caused extensive alterations in morphological features of erythrocyte and nuclear membranes and affected the permeability properties of rat liver mitochondrial membrane. It disrupted Ca2+ transport system and other energy dependent processes in mitochondria. A reduction in the activity of cytochrome-c-oxidase and NAD.H-oxidase was also observed.

Effect of acephate (orthene) on tissue levels of thiamine, pyruvic acid, lactic acid, glycogen and blood sugar.

Effect of Acephate, an organophosphorus insecticide, on tissue levels of thiamine, pyruvic acid, lactic acid, glycogen and blood sugar, has been studied. The albino rats, injected subcutaneously with Acephate (25 mg/10 gm body wt./day) for 4 weeks and 8 weeks, showed appreciable depletion of thiamine in liver, heart, kidney, brain and blood. The depletion of thiamine was found to be more after 8 weeks of Acephate injection. There was concomitant increase in pyruvic acid and lactic acid in various tissues. There was enormous depletion of glycogen in liver and slight rise in blood sugar concentration. The animals injected thiamine (120 micrograms/100 gm body wt./day) along with Acephate, showed more or less normal levels of thiamine, pyruvic acid, lactic acid, liver glycogen and blood sugar. The increase in pyruvic acid and lactic acid in tissues has been attributed to depletion of thiamine which is required of pyruvic acid oxidation. The increase in blood sugar has been attributed to the excess breakdown of glycogen.