The melon aphid, Aphis gossypii Glover (Hemiptera: Aphididae), is an important cosmopolitan and extremely polyphagous species capable of causing direct and indirect damage to various crops. Insecticide resistance in melon aphids is of particular concern. To determine the basis of resistance, organophosphate (OP)-resistant strains of A. gossypii were obtained by continuous selection with dimethoate in the laboratory, and resistance mechanisms were investigated along with susceptible strains. Three resistant strains LKR-1, LKR-2, and LKR-3 exhibiting 270-, 243-, and 210-fold resistance obtained after 30 generations of selection with dimethoate, respectively, were utilized in this study. The role of acetylcholinesterase (AChE), a target enzyme for OPs and carbamates (CMs), was investigated. AChE enzyme assay revealed that there was no significant change in the activities of AChE in resistant and susceptible strains. However, AChE inhibitory assay showed that 50% of the enzyme activity in resistant strains was inhibited at significantly higher concentration of dimethoate (131.87, 158.65, and 99.29 µmolL⁻¹) as compared with susceptible strains (1.75 and 2.01 µmolL⁻¹), indicating AChE insensitivity owing to altered AChE. Molecular diagnostic tool polymerase chain reaction-restriction fragment length polymorphism revealed the existence of two consistent non-synonymous point mutations, single-nucleotide polymorphism, viz., A302S (equivalent to A201 in Torpedo californica Ayres) and S431F (equivalent to F331 in T. californica), in the AChE gene Ace2 of resistant strains. Further, cloning and sequencing of a partial fragment of Ace2 (897 bp) gene from susceptible and resistant strains revealed an additional novel mutation G221A in resistant strains, LKR-1 and LKR-2. Susceptible Ace2 genes shared 99.6 and 98.9% identity at the nucleic acid and amino acid levels with resistant ones, respectively. Functional analysis of these point mutations was assessed by in silico docking studies using the modeled wild-type and naturally mutated AChE2. Computational analysis showed that the conformational changes in AChE2 active site due to structural gene substitutions (A302S, S431F, and G221A) significantly reduced the level of ligand (OP-dimethoate, omethoate, and CM-pirimicarb) binding, suggesting that they are potentially associated with resistance development. These results unambiguously suggested that multiple mutations located in the enzyme active site are responsible for AChE insensitivity to dimethoate and are likely the molecular basis for dimethoate resistance in these selected field populations of A. gossypii.

Aims: The aim of this study was to evaluate the antioxidant activty and anti-acid property of Acalypha wilkesiana foliage extract. Materials and Methods: Hot and cold aqueous extracts were prepared from healthy leaves of A. wilkesiana. Free radical scavenging activity and H ⁺ , K ⁺ -ATPase inhibition activities of aqueous foliage extracts was screened by in vitro models. Statistical Analysis Used: All experiments were performed in triplicate and results are expressed as mean ± SEM. Results: A. wilkesiana hot aqueous extract (AWHE) showed significant antioxidants and free radical scavenging activity. Further, AWHE has shown a potent H ⁺ , K ⁺ -ATPase inhibitory activity (IC ₅₀ : 51.5 ± 0.28 μg/ml) when compare to standard proton pump inhibitor omeprazole (56.2 ± 0.64 μg/ml); however, latter activity is equal to A. wilkesiana cold aqueous extract (AWCE). Quantitative analysis of AWHE has revealed more content of phenols and flavonoids; this is found to be the reason for good antioxidant activity over AWCE. Molecular docking was carried out against H ⁺ , K ⁺ -ATPase enzyme crystal structure to validate the anti-acid activity of A. wilkesiana major phytochemicals. Conclusions: The present study indicates that the constituents of AWHE and AWCE have good antacid and free radical scavenging activity.

Objective: The present study was undertaken to evaluate the possible ameliorative role of curcumin, capsaicin and their combination against lipopolysaccharide (LPS) induced hepatic toxicity in mice. Methods: Animals were distributed into five experimental groups: Normal control, vehicle control, curcumin, capsaicin and combined curcumin and capsaicin treatment groups respectively, for 7 days prior to LPS induced liver toxicity (3 mg/kg b.w. in saline). Hepatoprotective effect of individual and combined spice principles were evidenced by the measurement of serum marker enzyme activities such as, SGPT, ALP and TB and it was further confirmed by histopathological observation of liver tissue section. Results: The administration of LPS increased serum nonspecific enzymes (SGOT; 174.2±3.79 IU/L, SGPT; 124.0±3.14 IU/L, ALP; 320.15±3.88 IU/L and total bilirubin level; 2.32±1.23 mg/dL), however dietary curcumin and capsaicin decreased the activities of these non-specific serum enzymes including total bilirubin indicating amelioration of the severe LPS induced hepatotoxicity, while the combined spice principles were more significant as shown by the levels of enzymes activities SGOT; 89.9±1.39 IU/L, SGPT; 85.9±1.83 IU/L, ALP; 138.4±2.05 IU/L including total bilirubin level; 0.86±0.03 mg/dL. Conclusion: Dietary curcumin and capsaicin individually are protective to LPS induced hepatotoxicity, the beneficial effect was found to be more when the two compounds were fed in combination.