Evaluating the fate and potential health risks of organochlorine pesticides and triclosan in soil, sediment, and water from Asa Dam River, Ilorin Kwara State, Nigeria.

The quest for safe water due to exponential population growth and climate change has stressed the existing available water source. It is crucial to establish the present pollution level of the Asa River and the health risk it may pose to the people. Samples were collected along the Asa River, Ilorin, Kwara State, Nigeria, and treated using standard methods as stipulated by United States Environmental Protection Agency. The treated samples were analyzed and quantified for dieldrin, endrin, dichlorodiphenyltrichloroethane metabolites, mirex, hexachlorocyclohexane, hexachlorobenzene, and triclosan using the gas chromatography-mass spectrometry. The result showed that the levels of organochlorine pesticides (OCPs) ranged from 0.0045-0.947 µg/kg, 0.0036-0.093 µg/kg, and 0.001-0.007 µg/L in sediment, soil, and water samples, respectively. While the mean concentration of triclosan is 3.78 µg/kg, 2.995 µg/kg, and 0.064 µg/L in sediment, soil, and water samples, respectively. The levels of OCPs were lower than the limits in drinking water as set by World Health Organization and European Union. Health risk assessment for both children and adults was evaluated using non-carcinogenic and carcinogenic risk with the hazard quotient (HQ) and was found to be greater than unity (> 1) in children for the targeted OCPs. Associated cancer risk for OCPs ranged from low cancer risk to moderate risk for humans. The adverse ecological effects of OCPs showed to be very rare to occur and frequent effects may not likely occur except for HCH.

The human cancer cell active toxin Cry41Aa from Bacillus thuringiensis acts like its insecticidal counterparts.

Understanding how certain protein toxins from the normally insecticidal bacterium Bacillus thuringiensis (Bt) target human cell lines has implications for both the risk assessment of products containing these toxins and potentially for cancer therapy. This understanding requires knowledge of whether the human cell active toxins work by the same mechanism as their insecticidal counterparts or by alternative ones. The Bt Cry41Aa (also known as Parasporin3) toxin is structurally related to the toxins synthesised by commercially produced transgenic insect-resistant plants, with the notable exception of an additional C-terminal ß-trefoil ricin domain. To better understand its mechanism of action, we developed an efficient expression system for the toxin and created mutations in regions potentially involved in the toxic mechanism. Deletion of the ricin domain did not significantly affect the activity of the toxin against the human HepG2 cell line, suggesting that this region was not responsible for the mammalian specificity of Cry41Aa. Various biochemical assays suggested that unlike some other human cell active toxins from Bt Cry41Aa did not induce apoptosis, but that its mechanism of action was consistent with that of a pore-forming toxin. The toxin induced a rapid and significant decrease in metabolic activity. Adenosine triphosphate depletion, cell swelling and membrane damage were also observed. An exposed loop region believed to be involved in receptor binding of insecticidal Cry toxins was shown to be important for the activity of Cry41Aa against HepG2 cells.

Synthesis of novel heteroleptic delocalised cationic pyrazole gold complexes as potent HepG2 cytotoxic agents.

A new series of cationic gold(i) pyrazole complexes were prepared in excellent yields as their perchlorate salts. Results of cell viability assays show that these novel complexes have good cytotoxic properties against the human HepG2 cancer cell line. These complexes showed promising anti-cancer activities and to our knowledge, pyrazoles have never been tested against this cell line. The regioselectivity of the complexation is also discussed in regards to the substitution pattern of the pyrazoles.