Perfluoroundecanoic acid induces DNA damage, reproductive and pathophysiological dysfunctions via oxidative stress in male Swiss mice.

Perfluoroundecanoic acid (PFUnA) is an eleven carbon-chain compound that belongs to the perfluoroalkyl carboxylic acid family. It has been detected in the human blood, effluents, and surface/ground waters, but its toxic effects to the DNA and reproductive system remain unclear. This study was aimed at exploring the toxicity of PFUnA on the hepatic DNA, organ-system and reproductive system in orally treated male Swiss mice. In this present study, administration of PFUnA for 28 days with five doses (0.1, 0.3, 05, 0.7 and 1.0 mg kg-1 b.w./d) in male Swiss mice induced significant hepatic DNA damage which was observed using the alkaline comet assay and equally altered hematological and clinical biochemical parameters. In addition to testicular atrophy, sperm count and sperm motility significantly decreased while sperm abnormalities increased after 35 days exposure. Serum LH and FSH levels were remarkably increased while serum testosterone levels were strikingly reduced. Histopathology revealed the liver, kidney, and testis as potential targets of PFUnA toxicity. Increased activities of superoxide dismutase (SOD) and catalase (CAT), as well as levels of glutathione-s-transferase (GST) and reduced glutathione (GSH), with consistent reduction of glutathione peroxidase (GPx) and reduced glutathione (GSH) in the liver and testis induced oxidative stress. In conclusion, PFUnA exhibited both genotoxicity and reproductive toxicity via oxidative stress induction.

Exposure to effluent from pharmaceutical industry induced cytogenotoxicity, hematological and histopathological alterations in Clarias gariepinus (Burchell, 1822).

Pharmaceutical effluents contain toxic xenobiotics capable of contaminating aquatic environments. Untreated effluents are illegally discharged into aquatic environment in most developing countries. Pharmaceutical effluent induced alterations in biomarkers of genetic and systemic damage on rodents. However, information is relatively scarce on the possible cytogenotoxicity and systemic toxicity of this effluent on aquatic vertebrates. The study herein assessed the cytogenotoxic, hematological and histopathological alterations induced by pharmaceutical effluent in Clarias gariepinus. 96 h acute toxicity of the effluent was determined after C. gariepinus was exposed to six different concentrations (10 - 60 %) of the effluent. Subsequently, fish was exposed to sub-lethal concentrations (2.18 - 17.41 %) obtained from the 96 h LC50 for 7 and 14 days after which micronucleus (MN) and nuclear abnormalities (NAs) in peripheral erythrocytes were assessed as cytogenotoxic biomarkers, alterations in hematological indices and histopathological lesions were also examined. Fish, concurrently exposed to dechlorinated tap water and benzene (0.01 mL/L), served as negative and positive controls respectively. The derived 96 h LC50 of 17.41 % which was 1.89 times more toxic than the 24 h LC50 (32.95 %) showed that the effluent induced concentration-dependent mortality according to exposure duration. The effluent caused significant (p<0.05) time-dependent increase in the frequency of MN and abnormal nuclear erythrocytes compared to the negative control. Also, there was decrease in total erythrocyte counts, hemoglobin and hematocrit concentrations and increase in leucocyte and lymphocyte counts. The effluent induced pathological lesions on gills, liver and kidneys of treated fish. Higher physicochemical parameters than standard permissible limits in the effluent are capable of inducing genomic instability and systemic damage in fish. Pharmaceutical effluent can increase micropollutants in aquatic environmental and health risks to aquatic biota. There is need to promulgate stringent laws against illegal discharge of effluents into aquatic environment.

Correction to: Population data of 21 autosomal STR loci in the Hausa, Igbo and Yoruba people of Nigeria.

In the original paper author Alani Sulaimon Akanmu was erroneously omitted from the author list. Prof. Akanmu has now been added as 4th author. Prof. Akanmu acted as an academic supervisor of the study and additionally contributed to the publication by reading, commenting and editing the manuscript.

Population data of 21 autosomal STR loci in the Hausa, Igbo and Yoruba people of Nigeria.

The three major ethnic groups of Nigerian population namely the Hausa, Igbo and Yoruba make up 29, 21 and 18% of the total population, respectively. To provide genetic information necessary for forensic analysis, this study was carried out to determine STR allele frequencies in 102 Hausa, 128 Igbo and 134 Yoruba individuals in Nigeria using 21 STR loci including the 20 CODIS (Combined DNA Index System) loci plus SE33.

Identification of single nucleotide polymorphisms in the agouti signaling protein (ASIP) gene in some goat breeds in tropical and temperate climates.

The agouti-signaling protein (ASIP) plays a major role in mammalian pigmentation as an antagonist to melanocortin-1 receptor gene to stimulate pheomelanin synthesis, a major pigment conferring mammalian coat color. We sequenced a 352 bp fragment of ASIP gene spanning part of exon 2 and part of intron 2 in 215 animals representing six goat breeds from Nigeria and the United States: West African Dwarf, predominantly black; Red Sokoto, mostly red; and Sahel, mostly white from Nigeria; black and white Alpine, brown and white Spanish and white Saanen from the US. Twenty haplotypes from nine mutations representing three intronic, one silent and five missense (p.S19R, p.N35K, p.L36V, p.M42L and p.L45W) mutations were identified in Nigerian goats. Approximately 89 % of Nigerian goats carry haplotype 1 (TGCCATCCG) which seems to be the wild type configuration of mutations in this region of the gene. Although we found no association between these polymorphisms in the ASIP gene and coat color in Nigerian goats, in-silico functional analysis predicts putative deleterious functional impact of the p.L45W mutation on the basic amino-terminal domain of ASIP. In the American goats, two intronic mutations, g.293G>A and g.327C>A, were identified in the Alpine breed, although the g.293G>A mutation is common to American and Nigerian goat populations. All Sannen and Sahel goats in this study belong to haplotypes 1 of both populations which seem to be the wild-type composite ASIP haplotype. Overall, there was no clear association of this portion of the ASIP gene interrogated in this study with coat color variation. Therefore, additional genomic analyses of promoter sequence, the entire coding and non-coding regions of the ASIP gene will be required to obtain a definite conclusion.