The goal of this study was to assess biomarkers of exposure to glyphosate and assess potential associations with renal function in children. Glyphosate is used ubiquitously in agriculture worldwide. While previous studies have indicated that glyphosate may have nephrotoxic effects, few have examined potential effects on kidney function in children. We leveraged three cohorts across different phases of child development and measured urinary levels of glyphosate. We evaluated associations of glyphosate with three biomarkers of kidney injury: albuminuria (ACR), neutrophil gelatinase-associated lipocalin (NGAL), and kidney injury marker 1 (KIM-1). Multivariable regression analyses examined associations of glyphosate with kidney injury biomarkers controlling for covariates. We identified glyphosate in 11.1% of the total participants. The herbicide was detected more frequently in the neonate population (30%). Multivariable regression models failed to identify significant associations of log-transformed glyphosate with any of the kidney injury biomarkers, controlling for covariates age, sex, and maternal education. While we confirm detectability of glyphosate in children’s urine at various ages and stages of life, there is no evidence in this study for renal injury in children exposed to low levels of glyphosate. Further studies of larger sample size are indicated to better understand putative deleterious effects of the herbicide after different levels of exposure.

The purpose of the study was to determine Pb and Cd concentrations in humans and to assess the effect of co-exposure to these metals on biomarkers of oxidative stress and nephrotoxicity. Blood and urine levels of Pb and Cd, oxidative stress and urinary renal biomarkers were measured in 77 subjects neighboring a discharge and 52 in the control site. Exposed subjects showed significantly higher levels of lead and cadmium in blood and urine than the controls. Excessive production of reactive oxygen species induced by these metals in exposed subjects conducted to a decrease in antioxidant defense system (GPx, Selenium, GSH) and an increase in lipid peroxidation (MDA). Moreover, changes in markers of nephrotoxicity (high urinary concentrations of total protein, RBP and CC16, as well as GSTα and LDH increased activities) suggested the occurrence of discrete and early signs of impaired renal function for the discharge neighboring population.

Many studies using experimental and wild animals have reported negative effects of microplastic beads (MPs) ingestion. However, data regarding the lowest observed adverse effect levels (LOAELs) of MPs remain limited. Our aim was to evaluate the adverse effect levels of polyethylene MPs (10–63 μm diameter) with respect to growth, reproduction, and the eyes and kidneys of medaka (Oryzias latipes) under breeding conditions to contribute to future research involving LOAEL determinations. Fish were exposed to 0.009 mg-MPs (approximately 1000 particles)/L to 0.32 mg-MPs (approximately 40,000 particles)/L for 12 weeks. The eyes and kidneys were evaluated by histopathologic analysis. Although histologic analyses indicated an absence of MPs in the tissues, the eyes and kidneys as well as reproduction were adversely affected by increasing MP concentrations. The number of spawned eggs decreased, and changes were noted in the eyes of fish exposed to ≥0.032 mg-MPs/L under breeding conditions. The eyes exhibited thinning of the optic nerve fiber layer and dilatation of retinal capillaries compared with medaka not treated with MPs. Changes in the kidneys were observed in fish exposed to ≥0.065 mg-MPs/L. The mesangial matrix in the glomerulus of the kidneys was expanded compared with non-treated medaka, suggesting a deterioration in renal function. Analyses of an oxidative stress marker in the tissues indicated that lesion progression was associated with increased oxidative stress. Furthermore, a comparison of adverse effect levels suggested that MPs were more toxic to the eyes and reproduction than the kidneys or growth. Our data should prove useful for determining the LOAELs of polyethylene beads on vertebrates and enhance understanding of the mechanism underlying the biological toxicity of polyethylene MPs.

Exposure to phthalates is reported to be associated with increased incidence of microalbuminuria and low-grade albuminuria in children and adolescents. However, this phenomenon of phthalate-related nephrotoxicity is unknown in adults.Urine samples of 1663 adults from the 2012 Shanghai Food Consumption Survey (SHFCS) were measured for 10 metabolites of 6 phthalates and for renal function parameters. Their associations were explored by linear and logistic regression models.Multivariate linear regression analysis showed that all three renal function parameters (albumin-to-creatinine ratio (ACR), β2-microglobulin (B2M), and N-acetyl-β-d-glucosaminidase (NAG)) are positively associated with six metabolites, including mono-benzylphthalate (MBzP), mono-2-ethylhexylphthalate (MEHP), mono-2-ethyl-5-oxohexyphthalate (MEOHP), mono-2-ethyl-5-hydroxyhexylphthalate (MEHHP), mono-2-ethyl-5-carboxypentylphthalate (MECPP), and mono-2-carboxymethyl-hexyl phthalate (MCMHP) (P < 0.05). Logistic analysis showed that the prevalence of hyperALBuria, hyperB2Muria, hyperNAGuria, or potentially impaired renal function (PIRF) were positively associated with urinary levels of MBzP, MEOHP, and MECPP, respectively (P < 0.05). Co-exposure to identified risk metabolites monoethylphthalate (MEP), MBzP, MEHP, MEOHP, MECPP, MEHHP, and MCMHP increased the risk of having impaired renal function.Certain metabolites of phthalates, including bis (2-ethylhexyl) phthalate (DEHP) and benzyle butyl phthalate (BBzP), were associated with impaired renal function in Shanghai adults.

The purpose of the present study was to evaluate the possible ameliorative role of Thymus vulgaris (T. vulgaris) essential oil against Escherichia coli O157:H7 (E. coli O157:H7) deleterious effects in both blood and different tissues of rats by assessing the hematological, biochemical and immune-inflammatory parameters besides the histopathological alterations in the different organs. Forty male rats were randomly divided into four equal groups as follows: group I served as control, group II orally inoculated with E. coli O157:H7 at a dose of 1.0 × 10⁹ cfu/ml, group III orally received 250 mg/kg BW T. vulgaris oil daily for 7 days and group IV orally inoculated with E. coli O157:H7 as the same dose of group II and orally received T. vulgaris oil as the same dose and duration of group III. Bacterial challenge in groups II and IV was once at the beginning of experiment and administration of oil began after 72 h from bacterial inoculation. At the end of the study, blood was sampled and complete blood picture, liver and kidney function alongside immunoglobulins and cytokines concentrations were estimated and tissues of large intestine (colon), liver and kidneys were collected for histopathological examinations. The results revealed that there was an increase of red blood cells count, hematocrit value and hemoglobin concentration besides white blood cells and thrombocytes counts and substantial increment of serum markers of hepatorenal damage such as the activities of transaminases and concentrations of bilirubin (total, direct and indirect), total proteins, albumin, creatinine and urea in E. coli O157:H7-challenged group. Also, there was a considerable increase in serum immunoglobulins M and G, interleukin 6 and 8 and tumor necrosis factor alpha as well as decreased serum alkaline phosphatase activity. Moreover, T. vulgaris oil could partially improve the hematological, biochemical and histopathological alterations induced by E. coli O157:H7 without any significant alterations in all measured parameters when used alone. The study concluded that the T. vulgaris oil relatively diminished the alterations in hematological parameters, hepatic and renal function markers and immune-inflammatory variables alongside the histopathological changes in different organs induced by E. coli O157:H7. The ameliorative effects of T. vulgaris oil are mediated through its anti-inflammatory, antioxidant and immunomodulatory activities.

Exposures to cadmium and lead can cause oxidative stress, leading to tissue damage resulting in kidney and cardiovascular diseases. The antiaging protein klotho, on the other hand, is known to act as an anti-oxidative agent. How klotho homeostasis interacts with exposure to cadmium and lead has not been reported. Thus, this study was carried to investigate associations of serum klotho with blood and urine cadmium and lead in US adults aged 40–79 years across stages of eGFR-based kidney function and albuminuria defined as urinary albumin/creatinine ratio of > 30 mg/g creatinine. As long as the kidney function was normal (eGFR ≥ 90 mL/min/1.73 m²) or near normal (60 ≤ eGFR < 90 mL/min/1.73 m²), there was no evidence of an association between cadmium exposure and klotho concentrations irrespective of the presence/absence of albuminuria. During kidney dysfunction (15 ≤ eGFR < 60 mL/min/1.73 m²), 10% increases in blood cadmium concentrations resulted in decreases in klotho concentrations between 0.27 and 0.84%. In addition, during severe kidney dysfunction (15 ≤ eGFR < 45 mL/min/1.73 m²), a positive association between urine cadmium and serum klotho concentrations was observed. In the absence of albuminuria and when kidney function was normal or near normal, 10% increases in blood lead concentrations were observed to be associated with modest decreases between 0.28% and 0.37% in serum klotho concentrations. Similar results were observed between the concentrations of urine lead and serum klotho during kidney dysfunction.

Exposure to a single metal has been reported to damage renal function in humans. However, information regarding the association between multiple-metal exposure and markers for early renal impairment in different sexes among the young adult Taiwanese population is scarce. We assessed the association between exposure to arsenic (As), cadmium (Cd), and lead (Pb), and early renal impairment markers using urinary microalbumin (MA), β2-microglobulin (β2MG), and N-acetyl-beta-D-glucosaminidase (NAG) by analyzing 157 young adults aged 20‒29 years, in Taiwan. Inductively coupled plasma mass spectrometry was used to determine urinary As, Cd, and Pb levels. Regression models were applied to different sex groups. The results showed that after adjusting for potential confounding factors and each metal, urinary Cd levels were significantly positively associated with urinary MA (β = 0.523, 95% CI: 0.147–0.899) and β2MG (β = 1.502, 95% CI: 0.635–2.370) in males. However, the urinary Cd level was significantly positively associated with only urinary NAG (β = 0.161, 95% CI: 0.027–0.296) in females. This study thus indicates that the effect of exposure to metals (especially Cd) on early renal impairment among young adults in Taiwan is sex-specific. Our study results could contribute toward developing early intervention programs for decreasing the incidence of renal dysfunction. Further studies are warranted to confirm our findings and clarify the potential mechanisms involved.

This study assessed prophylactic potentials of silymarin against lead-induced hepatorenal toxicity in rats with the respect to its antioxidant and anti-apoptotic activities. Forty male albino rats were distributed into four groups. Control group is provided with distilled water. Lead acetate group was given lead acetate (100 mg/kg bwt) orally for 10 weeks. The third and fourth groups administered silymarin at doses of 50 or 100 mg/kg bwt, respectively, 1 h before administration of lead acetate for 10 weeks. Lead acetate altered liver structure and function that represented by significant elevation of the activities of serum aspartate and alanine aminotransferases and serum levels of urea and creatinine. Hepatic and renal tissues’ malondialdehyde concentrations were increased, while reduced glutathione content and superoxide dismutase and catalase activities were reduced in the lead acetate group. Also, lead acetate increased caspase-3 mRNA expression and inhibited alpha-fetoprotein mRNA expression in hepatic tissues, as well as it altered liver and kidney tissues’ architectures. In contrast, silymarin ameliorated in a dose dependent mannar the toxic effects of lead acetate on the liver and kidneys through modulation of lead acetate which altered liver and kidney function and structures via reducing lipid oxidation and pathological changes of hepatic and renal tissue structure, improving antioxidant defense system of liver and kidneys, and decreasing pro-apoptotic gene expression in hepatic tissue. This study indicated that silymarin ameliorated lead acetate-induced hepatorenal toxicity via its antioxidant and cytoprotective potentials.

Acrylamide (AA) is a hazardous chemical that is widely used in industrial practices. Spirulina platensis (SP) is a blue green alga that is rich in bioactive compounds with many medicinal benefits. The aim of the present study was to evaluate the ameliorative effect of SP against AA toxicity in rats. Animals were divided into six groups: Group (1) was normal rats, groups (2) and (3) received SP at 500 and 1000 mg/kg BW orally respectively for 21 days, group (4) was administered 20 mg/kg BW AA daily for 14 days, while groups (5) and (6) were given orally SP at the same doses of groups (2) and (3), then AA at similar dose of group (4). Rats that received AA alone displayed markedly increased serum levels of liver enzymes (ALT, AST, and ALP), kidney function parameters (urea and creatinine), DNA damage marker (8-OHdG), and proinflammatory cytokines (IL-1β, IL-6, and TNF-α), compared to control rats. Furthermore, tissue analysis revealed marked increases in hepatic, renal, and brain MDA and NO, as well as marked reductions in the antioxidant biomarkers (GSH, GSH-Px, SOD, and CAT) in acrylamide-intoxicated rats. Spirulina ameliorated the alterations in serum biochemical parameters and reduced MDA and NO, as well as improved antioxidant biomarkers in AA-intoxicated rats in a dose-dependent manner. Our results show that SP has a powerful protective effect on serum biochemistry and liver, kidney, and brain antioxidant machinery in AA-intoxicated rats.

Interest in phytochemical therapy methods in the treatment of diabetes is increasing day by day. Although the antidiabetic and antioxidant effects of Cistus laurifolius L. (CL) have been mentioned, the systemic effects remain unknown. The present study aims at evaluating the antidiabetic effects of the CL aqueous extract via metformin on streptozotocin (STZ)-induced diabetic rats. Forty male Wistar albino rats were divided into five groups of eight animals each: control, diabetic group (55mg/kg STZ), STZ+125mg/kg CL, STZ+250mg/kg CL, and STZ+100mg/kg metformin. The effects of CL and metformin on oxidative, apoptotic, and inflammatory pathways were comparatively investigated. In addition, nuclear factor-κB (NFκB), tumor necrosis factor-alpha (TNF-α), and interleukin (IL)-1β expressions analysis were carried out. CL treatment resulted in a significant improvement in blood glucose levels, lipid profile, pancreatic markers, and liver and kidney function tests. A 250mg/kg CL treatment decreased by 67.9%, 31.6%, 66.8%, 28.3%, and 31.4% in the total oxidant capacity, NFκB, TNF-α, IL-1β, caspase3, and cytochrome c levels, respectively, compared to the diabetic group. Additionally, CL treatments showed a dose-dependent reduction in NFκB, TNF-α, and IL-1β expression levels. A 250mg/kg CL treatment exhibited a greater increase (by 9.6%) in total antioxidant capacity than metformin. CL treatment provided histologically more improvement in the brain, heart, pancreas, spleen, liver, kidney, and testicular tissues compared to the metformin group. Our results suggest that the single treatment of CL aqueous extract at the low doses may have stronger short-term anti-diabetic effects than metformin. Therefore, further studies are needed regarding the long-term hypoglycemic effect or treatment of CL aqueous extract.