David Ebuka Arthur

A review on the assessment of polymeric materials used as corrosion inhibitor of metals and alloys

Corrosion control of metals is an important activity of technical, economical, environmental, and aesthetical importance. The use of inhibitors is one of the best options of protecting metals and alloys against corrosion. The toxicity of organic and inorganic corrosion inhibitors to the environment has prompted the search for safer corrosion inhibitors such as green corrosion inhibitors as other more environmental friendly corrosion inhibitors, most of which are biodegradable and do not contain heavy metals or other toxic compounds. Investigations of corrosion-inhibiting abilities of polymeric substances, e.g., plant gums, in addition to being environmentally friendly and ecologically acceptable, have shown that plant products are inexpensive, readily available, and renewable sources of materials. Need for more effective inhibitors has propelled companies such as the Montazhkhimzashchita Trust to develop a pool method of welding sheet vinyl, a method widely employed in gluing on roller sticky bands from thermoplast on a pipe. The article enumerates several kinds of polymeric materials which are suitable for use in combating corrosion, and several which have suitable strength characteristics as to serve in place of scarce expensive metals and alloys.

The role of molecular modelling strategies in validating the effects of chrysin on sodium arsenite-induced chromosomal and DNA damage:

Chrysin (CHR) is a food-based bioactive ingredient whereas, sodium arsenite (SA) is one of the major contaminant in drinking water. When ingested, SA contributes to tissue damage due to bioactivation by S-adenosyl methionine (SAM)-dependent methyltransferase. Hence, the needs to nullify this effect by investigating the potentials of CHR on SA-induced genotoxicity in rats. The experiment was divided into two successive stages (ameliorative and preventive, curative studies) for 1 week. Rats were divided into four groups: distilled water, 10mg/kg SA, 10mg/kg CHR and co-administration. In stage 2, the experimental groups were given either CHR or SA for 1 week, and treated in reversed order for additional week. Lipid peroxidation, protein carbonyl and DNA fragmentation in liver, blood brain and bone marrow cells micronucleus were assayed for using standard protocols. Molecular docking of SAM-dependent methyltransferase in the presence of CHR was conducted. CHR significantly (p < 0.05) decreased the level of lipid peroxidation, protein carbonyls and DNA fragmentation in blood, liver and brain tissues as against group treated with SA. It also significantly (p<0.05) reduced the level of micronuclei generated in bone marrow cells. The effects of CHR were shown to be ameliorative, preventive and curative in nature. Furthermore, CHR was able to dock (with binding energy of −24.81 kcal/mol and predicted inhibition kinetic constant (Ki) of 0.959 µM) into the active site of SAM-dependent methyltransferase with strong hydrogen bond and hydrophobic interactions. The study might have unravelled the potentials of CHR against SA-induced chromosomal and DNA damage, which might be due to inhibition of SAM-dependent methyltransferase.

In silico modelling of quantitative structure–activity relationship of multi-target anticancer compounds on k-562 cell line

The pGI50 cytotoxicity values of 112 compounds on K-562 cancer cell line were modeled to illustrate the quantitative structure–activity relationship (QSAR) of the compounds. The dataset were divided into training and test set through Kennard-stone algorithm, while the pool of molecular descriptors calculated with paDEL descriptor metric program was subjected to the genetic functional algorithm (GFA) for selection of descriptor to be modeled. The best QSAR model developed was then subjected to a rigorous statistical test. The statistical significance of the model was verified by calculating the values of Q2LOO (0.845), Q2F1 (0.9397), Q2F2 (0.6862) and R2pred (0.6862) needed to evaluate the strength and robustness of the model. The result of the internal and external validation of the model indicates that the model is good and could be used to predict the GI50 of anticancer compounds on K-562 leukemia cell line. The model developed was used in designing new anticancer drugs with higher activity or more potent and less toxic in nature when compared to the lead compound. These compounds significant activities were found to correlate to with some of the molecular descriptors such as the number of hydrogen bond acceptors present in the surface of the molecule.

Modulatory role of rutin on 2,5-hexanedione-induced chromosomal and DNA damage in rats: validation of computational predictions

Abstract The aim of this study was to evaluate the potentials of rutin on 2,5-hexanedione-induced toxicities. Two successive phases were involved using in silico and in vivo approaches. The in silico was adopted for potential oral toxicity and docking. The in vivo was carried-out in two stages for two weeks; the ameliorative (stage 1, first week), preventive, and curative studies (stage 2, extended to second week). In stage 1, rats were divided into four groups of seven each (distilled water, 3% (v/v) 2,5-hexanedione, 10 mg/kg rutin, and co-administration). In stage 2, the experimental groups were given either rutin or 2,5-hexanedione and treated in reverse order. Lipid peroxidation, protein carbonyl, and DNA fragmentation in tissues and bone marrow cells micronucleus were determined. The predicted Median lethal dose (LD50) of >5000 mg/kg and toxicity class of five (5) indicates the safety of rutin when orally administered. 2,5-Hexanedione comfortably docked in to the active sites of SOD (−22.857Kcal/mol; KI = 0.9621 µM), GPx (−11.2032Kcal/mol; KI = 0.9813 µM), and CAT (−16.446Kcal/mol; KI = 0.9726 µM) with strong hydrogen bond and hydrophobic interactions. However, only strong hydrophobic interaction was observed in the case of DNA (−3.3296Kcal/mol; KI = 0.9944). In vivo findings revealed deleterious effects of 2,5-hexanedione through induction of oxidative and chromosomal/DNA damage characterized by higher level of malondialdehyde, micronuclei formations, and DNA fragmentation. These have invariably, validates the findings from in silico experiments. Furthermore, rutin was able to ameliorate, protect, and reverse these effects, and was relatively non-toxic corroborating toxicity predictions. Rutin exhibited counteractive effects on 2,5-hexanedione-induced oxidative, chromosomal, and DNA damage.

Insilico Modelling of Quantitative Structure-Activity Relationship of Pgi50 Anticancer Compounds on k-562 Cell Line

Abstract The pGI50 cytotoxicity values of 112 compounds on K-562 cancer cell line were modelled in order to illustrate the quantitative structure–activity relationship of the compounds. The data set were divided into training and test set through Kennard-stone algorithm, while the pool of molecular descriptors calculated with paDEL descriptor metric program was subjected to genetic functional algorithm for selection of descriptor to be modeled. The statistical significance of the model was verified by calculating the values of Q2LOO (0.845), Q2F1 (0.9397), Q2F2 (0.6862) and R2pred (0.6862) needed to evaluate the strength and robustness of the model. The result of the internal and external validation of the model indicates that the model is good and could be used to predict the GI50 of anticancer compounds on K-562 leukemia cell line.