Effect of Silver-Containing Titania Layers for Bioactivity, Antibacterial Activity, and Osteogenic Differentiation of Human Mesenchymal Stem Cells on Ti Metal.

Biomaterials with better osteogenic capacity, rapid osteo-integration, and higher mechanical strength are undoubtedly preferred for successful bone implant development. A porous sodium hydrogen titanate layer was formed on Ti metal by NaOH treatment, and the Na+ ions were replaced by Ag+ ions by subsequent AgNO3 treatment that formed silver-containing hydrogen titanate. Heat treatment at 600 °C transformed sodium hydrogen titanate into sodium titanate with sheet-like morphology, whereas silver-containing hydrogen titanate was converted to anatase TiO2 with an elongated rod-like structure. Further increment in temperature lead to the formation of rutile TiO2 with distracted network morphology. Between these two, the anatase TiO2 was ascertained to be bioactive by being capable of forming bonelike apatite in simulated body fluid within a period of 12 h. The concentration of silver on Ti metal was further optimized for better antibacterial activity against S. aureus and biocompatibility toward bone cells. A detailed investigation of thus optimized silver-containing Ti metal on the proliferation and differentiation of multipotent human mesenchymal stem cells further proved their biocompatibility nature and facilitation of osteogenic differentiation, thereby conferring those as ideally suited materials for bioimplant development in bone tissue engineering.

Disposition and acute toxicity of imidacloprid in female rats after single exposure.

Single dose of imidacloprid (IMI-20mg/kg bodyweight) was orally administered in female rats. Its disposition along with two metabolites 6-chloro nicotinic acid (6-CNA) and 6-hydroxy nicotinic acid (6-HNA) was monitored in organs (brain, liver, kidney, and ovary) and bodily fluids (blood, urine) at 6, 12, 24 and 48h and faeces at 24 and 48h. Maximum concentration (Cmax) of IMI and metabolites in each organ and bodily fluid occurred after 12h. Area under curve (AUC) of IMI ranged from 35 to 358µg/ml/h; 6-CNA: 27.12-1006.42µg/ml/h and 6-HNA: 14.98-302.74µg/ml/h in different organs and bodily fluids. Clearance rate of IMI was maximum in ovary followed by kidney, liver, brain, faeces, blood and urine. Percent inhibition of acetyl-cholinesterase (AChE) was comparable in brain and Red Blood Cells (RBC) at 6-48h which suggests the RBC-AChE as valid biomarker for assessing IMI exposure. It is evident that IMI was absorbed, metabolized, and excreted showing increased level of serum enzymes like Glutamic oxaloacetic transaminase (GOT), Glutamic pyruvic transaminase (GPT) and biochemical constituents like billirubin and Blood Urea Nitrogen (BUN) at 48h. These data suggest that IMI is widely distributed, metabolized and induced toxicology effects at 20mg/kg bodyweight to female rats.

Analysis of imidacloprid residues in fruits, vegetables, cereals, fruit juices, and baby foods, and daily intake estimation in and around Lucknow, India.

A total of 250 samples-including fruits, fruit juices, and baby foods (50 samples each), vegetables (70 samples), and cereals (30 samples)-were collected from Lucknow, India, and analyzed for the presence of imidacloprid residues. The QuEChERS (quick, easy, cheap, effective, rugged, and safe) method of extraction coupled with high-performance liquid chromatographic analysis were carried out, and imidacloprid residues were qualitatively confirmed by liquid chromatography-mass spectrometry. Imidacloprid was not detected in samples of fruit juices and baby foods. It was, however, detected in 38 samples of fruits, vegetables, and cereals, which is about 15.20% of the total samples. Of samples of fruits, 22% showed the presence of imidacloprid, and 2% of samples showed residues above the maximal residue limit. Although imidacloprid was detected in 24% of vegetable samples, only 5.71% showed the presence of imidacloprid above the maximal residue limit. However, 33% of cereal samples showed the presence of imidacloprid, and about 3% of samples were above the maximal residue limit. The calculated estimated daily intake ranged between 0.004 and 0.131 µg/kg body weight, and the hazard indices ranged from 0.007 to 0.218 for these food commodities. It is therefore indicated that lifetime consumption of vegetables, fruits, fruit juices, baby foods, wheat, rice, and pulses may not pose a health hazard for the population of Lucknow because the hazard indices for imidacloprid residues were below one.

Toxicological impact of technical imidacloprid on ovarian morphology, hormones and antioxidant enzymes in female rats.

Technical imidacloprid was evaluated for its effect on ovarian morphology, hormones and antioxidant enzymes in female rats after 90 days oral exposure. Luteinizing hormone (LH), follicle stimulating hormone (FSH) and progesterone levels were estimated in serum of rats and activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and level of reduced glutathione (GSH) and lipid peroxidation (LPO) were estimated in ovary after oral administration of imidacloprid (5, 10, and 20mg/kg/day) for 90 days. Decreased ovarian weight together with significant patho-morphological changes in follicles, antral follicles and atretic follicles were observed at 20mg/kg/day. Imidacloprid at 5 and 10mg/kg/day has not produced any significant changes in ovarian morphology, hormones and antioxidant status of ovary. However 20mg/kg/day dose has produced significant alterations in the levels of LH, FSH and progesterone. Similarly significant changes in SOD, CAT, GPx, GSH, and LPO were observed at 20mg/kg/day dose level. Therefore, it is concluded that imidacloprid at 20mg/kg/day dose level has produced significant toxicological impact on ovary of female rats as evident by pathomorphological changes, hormonal imbalance and generating oxidative stress and can be considered primarily as Lowest Observed Effect Level (LOEL) for chronic study.

A 90 days oral toxicity of imidacloprid in female rats: morphological, biochemical and histopathological evaluations.

A 90 days oral toxicity study of imidacloprid was conducted in female rats with doses of 0, 5, 10, 20mg/kg/day. Decrease in the body weight gain was observed at 20mg/kg/day and at necropsy the relative body weights of liver, kidney and adrenal was also significantly increased at this dose level. No mortality occurred during treatment period while food intake was reduced at high dose level. In clinical chemistry parameters high dose of imidacloprid has caused significant elevation of serum GOT, GPT, glucose and BUN and decreased the activity of AChE in serum and brain. The spontaneous locomotor activity was also decreased at highest dose exposure where as there were no significant changes in hematological and urine parameters. The brain, liver and kidney of rats exposed with high dose of imidacloprid had showed mild pathological changes. Based on the morphological, biochemical, hematological and neuropathological studies it is evident that imidacloprid has not produced any significant effects at 5 and 10mg/kg/day doses but induced toxicological effects at 20mg/kg/day to female rats. Hence, 10mg/kg/day dose may be considered as no observed effect level (NOEL) for female rats.

Effect of imidacloprid on antioxidant enzymes and lipid peroxidation in female rats to derive its No Observed Effect Level (NOEL).

Technical imidacloprid was evaluated for its effect on oxidative stress and Lipid peroxidation (LPO) in female rats for No Observed Effect Level (NOEL). Activities of Superoxide dismutase (SOD), Catalase (CAT), Glutathione peroxidase (GPx), and level of Glutathione (GSH) and LPO were estimated in liver, kidney and brain of rats after oral administration of imidacloprid (5, 10, 20 mg/kg/day) for 90 days. Imidacloprid at 5 and 10 mg/kg/day has not produced changes in SOD, CAT, GPx and level of GSH and LPO in liver, brain and kidney. However 20 mg/kg/day has produced significant changes in SOD, CAT, GPx, GSH, LPO in liver; SOD, CAT and GPx in brain and LPO in kidney. Therefore, it is concluded that imidacloprid has not generated oxidative stress at 5 and 10mg/kg/day but induced changes at 20 mg/kg/day. Hence 10 mg/kg/day may be considered as NOEL through antioxidant enzymes and LPO in female rats.