Label information, nutritional composition and screening for bromate in breads sold in Umuahia, Abia State, Nigeria

Non-use of potassium bromate in bread making and printing of reproducible nutrition information/claims on bread labels are vital for consumers’ rights and protection in Nigeria. These norms are rarely observed by bread makers in Umuahia. This study evaluated nutrition information on labels, presence of potassium bromate, chemical composition and sensory characteristics of breads sold in Umuahia. Two structured questionnaires were constructed. The first was administered to 15 randomly selected full-time bread vendors in Umuahia metropolis to identify brands of market bread. The second was designed to analyze sensory quality of breads. Five sliced and five unsliced bread samples randomly selected from identified markets were analyzed for sensory properties using a 20-member sensory panelist, and for nutrient and phytochemical composition. Twenty-seven bread samples were identified; all labeled bromate-free, had varying recipes and nutrient claim/information on labels. The bread samples were bromate-free, high in carbohydrate (49.20% in B10 to 65.69% in B8) and moisture (22.67% in B8 to 38.16% in B10), but relatively low in crude protein (6.65% in B3 to 9.45% in B7) and fat (0.26% in B8 to 0.66% in B1). Ash contents ranged from 1.26% in B6 to 1.86% in B3and fiber contents from 1.24% in B2 to 1.76% in B5. Phytonutrients were low; and oxalate content ranged from 0.66 to 0.95%, tannin from 87.78 to 125.40 mg 100g–1 and phytate from 2.02 to 3.03 mg 100g–1. The bread samples had sensory scores ranging from 4.60 to 8.10 for over-all acceptability. They were all acceptable to panelists, but with B1 (sliced) and B8 (unsliced) most acceptable. Bread samples sold in Umuahia were bromate-free, varied in recipe, nutrition claims, and nutrient composition but were acceptable to panelists.

Characteristic mutations induced in the small intestine of Msh2-knockout gpt delta mice

Background Base pair mismatches in genomic DNA can result in mutagenesis, and consequently in tumorigenesis. To investigate how mismatch repair deficiency increases mutagenicity under oxidative stress, we examined the type and frequency of mutations arising in the mucosa of the small intestine of mice carrying a reporter gene encoding guanine phosphoribosyltransferase (gpt) and in which the Msh2 gene, which encodes a component of the mismatch repair system, was either intact (Msh2+/+::gpt/0; Msh2-bearing) or homozygously knockout (KO) (Msh2−/−::gpt/0; Msh2-KO). Results Gpt mutant frequency in the small intestine of Msh2-KO mice was about 10 times that in Msh2-bearing mice. Mutant frequency in the Msh2-KO mice was not further enhanced by administration of potassium bromate, an oxidative stress inducer, in the drinking water at a dose of 1.5 g/L for 28 days. Mutation analysis showed that the characteristic mutation in the small intestine of the Msh2-KO mice was G-to-A transition, irrespective of whether potassium bromate was administered. Furthermore, administration of potassium bromate induced mutations at specific sites in gpt in the Msh2-KO mice: G-to-A transition was frequently induced at two known sites of spontaneous mutation (nucleotides 110 and 115, CpG sites) and at nucleotides 92 and 113 (3′-side of 5′-GpG-3′), and these sites were confirmed to be mutation hotspots in potassium bromate-administered Msh2-KO mice. Administration of potassium bromate also induced characteristic mutations, mainly single-base deletion and insertion of an adenine residue, in sequences of three to five adenine nucleotides (A-runs) in Msh2-KO mice, and elevated the overall proportion of single-base deletions plus insertions in Msh2-KO mice. Conclusions Our previous study revealed that administration of potassium bromate enhanced tumorigenesis in the small intestine of Msh2-KO mice and induced G-to-A transition in the Ctnnb1 gene. Based on our present and previous observations, we propose that oxidative stress under conditions of mismatch repair deficiency accelerates the induction of single-adenine deletions at specific sites in oncogenes, which enhances tumorigenesis in a synergistic manner with G-to-A transition in other oncogenes (e.g., Ctnnb1).

Potassium bromate-induced nephrotoxicity and potential curative role of metformin loaded on gold nanoparticles

Potassium bromate (KBrO3) is classified by the International Agency for Research on Cancer as a carcinogenic compound, where it causes renal tumors. The present study investigated the potential curative effect of metformin loaded on gold nanoparticles (MET AuNPs) in attenuating KBrO3-induced nephrotoxicity. Rats were divided into eight groups (control, MET, AuNPs, MET AuNPs, KBrO3, KBrO3/MET, KBrO3/AuNPS, and KBrO3/MET AuNPs). KBrO3 administration resulted in a significant elevation in serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), total protein (TP), albumin (Alb), total bilirubin (TB), direct bilirubin (DB), total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), creatinine, urea, uric acid. Also, KBrO3 significantly increased renal malondialdehyde (MDA), protein carbonyl (PC), and nitric oxide (NO) levels and reduced the activities of antioxidant molecules superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), and Reduced glutathione (GSH). It also caused damaged DNA spots in comet assay and increased inflammatory IL-6 and apoptotic markers (caspase 3, Bax) while antiapoptotic Bcl-2 was significantly reduced. MET, AuNPS, MET AuNPS reduced the extent of renal damage induced by KBrO3 as indicated by decreased (AST, ALT, ALP, Alb, TP, TB, DB, creatinine, urea, uric, Lipid profile). MET, AuNPS, MET AuNPS showed a good curative effect against KBrO3-induced nephrotoxicity and MET AuNPS group showed better results compared with monotherapy.

Effect of Ethanol Extract of Aframomum angustifolium Seed on the Induction of Nephrotoxicity by Bromate in Wistar Rats

Background: The continued use of bromate due to its oxidizing property poses health hazards since it is an established nephrotoxic agent. Objectives: This study evaluated the capacity of the ethanol extract of Aframomum angustifolium seeds to ameliorate the nephrotoxicity of potassium bromate in Wistar rats. Methods: In stage I of this study, the main phytochemical groups in the seeds were quantified using spectrophotometric procedures. The acute and sub-chronic toxicities of the extract were studied by monitoring physical and biochemical parameters in stage II. In stage III, the reno-protective effect of the extract were determined by administering 350 and 750 mg/kg bw of the extract with 30 mg/kg bw potassium bromate orally. The reno-protective study lasted for 56 days and the effect of treatment on biomarkers was determined on days 28 and 56. Results: The phytochemical groups (i.e., alkaloids, flavonoids, saponins, tannins, ascorbic acid, and alpha-tocopherol) were detected in the seeds. The acute and sub-chronic oral administration of the extract did not induce any significant toxic reactions across the studied concentrations. The sub-chronic administration of the extract reduced average weight gain in the treated groups. The obtained results in the reno-protective and histological studies indicated that the seed extract offers protection against the induced oxidative assault by bromate. Conclusion: In general, the co-administration of the ethanol extract of A. angustifolium seeds with bromate can reduce its nephrotoxicity in a dose-dependent manner.