Evaluation of heavy metal contaminants in prepared noodles: source allocation and health risk assessment.

In recent years, special attention has been given to emission research that led to the deposition of toxicants from road traffic. Thus, it is imperative to focus on heavy metal (HM) stressors in food items, their source contribution, and health risk assessment providing insight into their spatial role at the population level. In this study, heavy metal in the street vended noodles was studied while correlating the quality of noodle with different environmental origins. The samples were prepared using acid digestion and analysed by flame atomic absorption spectrophotometer, except Hg which was analysed by direct mercury analyser. The results showed that some heavy metals like Cr, Pb, Mn, Cd, and Hg exceed their permissible limits established by the international legislation for food products. In the noodle samples, the concentration of heavy metal ranged from < 0.1 to 0.904 mg/kg for Pb, < 0.09 to 0.843 mg/kg for Ni, < 0.004 to 0.201 mg/kg for Cd, < 0.0001 to 0.004 mg/kg for Hg, < 0.01 to 1.388 mg/kg for Cu, < 0.015 to 8.049 mg/kg for Mn, and < 0.02 to 16.514 mg/kg for Cr. Noodle samples vended on high traffic density streets are directly associated with increased HM content due to atmospheric deposition from the surrounding. Source apportionment study determines that HM contamination belongs to the same source of origin, except Cr. Based on the cluster analysis, these samples fall into three major groups that were further validated by the canonical discriminant function. Health risk prediction by Monte Carlo simulation revealed an elevated non-carcinogenic health hazard risk to consumers with a hazard index (HI) shift from 71 to 75%. Health hazard analysis showed that consumers of high traffic density street vended food are at higher risk of developing health-related issues. This study is important to evaluate the health risk of the population exposed to heavy metals due to ingestion of street vended food.

Ochratoxin A treated rat derived urinary exosomes enhanced cell growth and extracellular matrix production in normal kidney cells through modulation of TGF-ß1/smad2/3 signaling pathway.

AIMS: Kidney is the main target organ for ochratoxin A (OTA) toxicity; however, the mechanism(s) involved in OTA-induced nephrotoxicity is not fully understood. Recently, exosomes, nano-sized vesicles have been found to play an important role in promotion and progression of disease as well as environmental toxicant-induced patho-physiology of toxicity. Hence, we aimed to investigate the role of exosomes in OTA-mediated nephrotoxicity. MAIN METHODS: Male Wistar rats were divided in to two groups. Rats of one group were treated with OTA (210 µg/kg b. wt) and another with vehicle control through oral gavage (5 days/week) for 270 days. At the end of experiment, exosomes concentrations from rat's urine were measured. To examine the OTA-induced nephrotoxicity, histopathology was performed using H & E, Masson's trichome and PAS staining. For mechanistic study, normal rat kidney (NRK52E) cells were exposed with either vehicles treated rat's urinary exosomes (NEx) or OTA treated rat's urinary exosomes (OEx) and effects on cell proliferation, cell growth, extracellular matrix production and TGF-ß1/smad2/3 pathway was analyzed. KEY FINDINGS: OTA treatment to Wistar rats caused histopathological changes such as tubular degeneration, glomeruli shrinkage and hypercellularity in kidney tissue. Interestingly, OTA treated rat's urine has more exosomes secretion. Moreover, treatment of NRK52E cells with OEx caused increased cell proliferation, cell growth, enhanced the expression of extracellular matrix proteins and activation of TGF-ß1/smad2/3 pathway. SIGNIFICANCE: Our investigations exogenous exposure of OTA derived urinary exosomes caused TGF-ß1/smad2/3 pathway-mediated activation of pro-fibrotic changes in kidney will helpful for deeper understanding the OTA-induced nephrotoxicity.

Cobalt oxide (Co3O4) nanoparticles induced genotoxicity in Chinese hamster lung fibroblast (V79) cells through modulation of reactive oxygen species.

Incessant production, pervasive applications in different fields, and eventually unintended exposure of cobalt oxide nanoparticles (Co3O4 NPs) lead to rise in their toxicity studies toward human health. However, the information regarding the potential toxicity mechanisms of Co3O4 NPs especially genotoxicity is still sparse with missing interconnections. So far, only solitary reports on Co3O4 NPs are at hand, bearing witness to reactive oxygen species (ROS)-mediated DNA damage in lung cells. To address this, we evaluated the Co3O4 NP-induced cytotoxic and genotoxic potential in Chinese hamster lung fibroblast cell line (V79). Our preliminary results demonstrate that Co3O4 NPs at concentrations of 20-100 µg/ml induced moderate mortality after 24-h exposure. However, these low concentrations caused a significant reduction in various organelles' activity in a concentration-dependent manner. Mitochondrial activity and membrane potential were found to be compromised due to NP exposure in a concentration-dependent manner. The study affirms that Co3O4 NPs inhibited lysosomal activity in V79 cells. In addition to this, Co3O4 NPs are also found to stimulate free oxygen radical generation. Genotoxicity studies revealed a potent and dose-dependent effect of non-cytotoxic concentrations of Co3O4 NPs in the induction of DNA lesions. Interestingly, N-acetylcysteine, a free oxygen radical scavenger (5, 10 mM, pretreatment) inhibited the progression of free oxygen radicals and induction of Co3O4 NP-mediated DNA lesions. This suggests the ROS-mediated genotoxic potential of Co3O4 NPs.

Evaluation of Antithrombotic Activities of Solanum xanthocarpum and Tinospora cordifolia.

BACKGROUND: Solanum xanthocarpum and Tinospora cordifolia have been reported to exhibit anti-inflammatory, antiarthritic, antioxidant, antiallergic, and hepatoprotective activities. The origins of many of the currently available antithrombotic treatments are from natural products and natural sources. OBJECTIVE: To investigate the antithrombotic activities of methanolic leaf extracts of S. xanthocarpum(SXME) and T. cordifolia(TCME). MATERIALS AND METHODS: Antithrombotic activities were assessed by thrombin inhibition assay, thrombin generation assay, platelet adhesion assay on collagen-coated surface, and platelet PAC1-FITC binding by flow cytometry. RESULTS: SXME significantly inhibited thrombin activity at 5-20 mg/ml concentrations, whereas TCME inhibited thrombin activity at 500 µg/ml-5 mg/ml concentrations. Further, SXME inhibited thrombin generation at 2-20 mg/ml concentrations, whereas TCME exhibited significant inhibition at 200 µg/ml, suggesting that TCME has higher efficacy as compared to SXME. Moreover, SXME did not inhibit platelet adhesion on collagen-coated surface, whereas TCME inhibited platelet adhesion on collagen-coated surface at 5 mg/ml. Indomethacin showed significant inhibition in platelet adhesion at 300 µM. Further, SXME inhibited thrombin-induced platelet activation (PAC1-FITC binding) significantly at 1 mg/ml by about 80%, whereas TCME inhibited thrombin-induced platelet activation (PAC1-FITC binding) by about 40% at 1 mg/ml. CONCLUSION: These results strongly suggested that SXME and TCME possess antithrombotic activities. However, further studies are essential to find out the active constituent responsible for antithrombotic effect. SUMMARY: The methanolic extracts obtained from the leaves of Tinospora cordifolia and Solanum xanthocarpum were evaluated for antithrombotic activity by thrombin inhibition assay, thrombin generation assay, platelet adhesion assay and platelet activation assay by flow cytometry. These extracts inhibited thrombin activity and thrombin generation in rat plasma. Also, these extracts inhibited thrombin induced platelet activation in PAC1-FITC binding study in flow cytometry. Abbreviation Used: DVT: Deep vein thrombosis, TCME: Tinospora cordifolia methanolic extract, SXME: Solanum xanthocarpum methanolic extract, IL-1ß: interleukin-1ß, DMSO: dimethyl sulfoxide, PRP: Platelet rich plasma.