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Exposure to metal dust is a significant occupational hazard for foundry workers. This study aimed to investigate exposure to potentially toxic metals and oxidative stress indices and assess the health risk of occupational exposure to metal dust among foundry workers. Environmental and biological exposures to a cocktail of metals were examined by measuring the concentration of Aluminum (Al), Zinc (Zn), Copper (Cu), Cadmium (Cd), Nickel (Ni), and Chromium (Cr) in the air of the workplace, as well as in the blood of the exposed workers. Malondialdehyde (MDA), reduced blood glutathione (GSH) and urinary 8- hydroxydeoxy guanosine (8-OH-dG) were measured as biomarkers of oxidative stress. All air measurements were below the maximum allowable limits (MAL) except for Al and Ni according to American Conference of Industrial Hygienists (ACGIH) and National Institute of Occupational Safety and Health (NIOSH). Here is significantly elevated Blood Al, Zn, Cu, and Pb levels in exposed workers. Moreover, MDA and 8-OHdG levels significantly increased (P<0.0001). In contrast, the mean level of GSH was reduced considerably in exposed workers compared to the control group (P<0.0001). The MDA acts as a marker with the highest Area Under the Curve (AUC), enabling effective differentiation between the exposed and control subjects (AUC = 0.968; Sensitivity = 90%, Specificity =100%; P <0.0001). Workers occupationally exposed to these metals for prolonged periods possessed higher metal levels in their bodies, which is associated with increased oxidative stress, which consequently causes DNA damage. [ABSTRACT FROM AUTHOR]

Hyperuricemia was linked to diabetes mellitus, metabolic syndrome, and oxidative stress, and could be induced by higher fructose consumption through altering energy status in liver. l‐Carnitine is an antioxidant, affecting mitochondria and cellular energetics; however, little is known about its effects in hyperuricemic states. This study investigated metabolic and hepatic effects of hyperuricemia and fructose feeding, and demonstrated the role of l‐Carnitine in such states. Fifty adult male Wistar rats were randomly divided into control, untreated hyperuricemic, fructose‐supplemented hyperuricemic, l‐Carnitine‐treated hyperuricemic, and l‐Carnitine‐treated fructose‐supplemented hyperuricemic groups. The separated plasma was used for determination of the glycemic control, lipid profile, liver function tests, uric acid level, and oxidative stress markers. Atherogenic index, HOMA‐IR, and body mass index (BMI) were calculated. Left liver lobe and left kidney specimen from all groups were used for histopathological studies. Hyperuricemic rats exhibited significantly hypoalbuminemia, dyslipidemia, insulin resistance, and oxidative stress compared to the controls. Fructose‐supplemented hyperuricemic group showed obesity and more deleterious effects, as well as, steatosis, and renal tubular damage compared to the hyperuricemic rats. Concomitant l‐Carnitine treatment with hyperuricemia improved such effects, despite causing adiposity. While combined l‐Carnitine treatment and fructose supplementation in hyperuricemia limited the aggressive hyperuricemic picture of fructose supplementation. It is concluded that hyperuricemia has detrimental metabolic and hepatic effects. Artificial fructose supplementation worsened such effects, while l‐Carnitine was efficient in ameliorating these hyperuricemia and/or excess fructose‐induced hyperuricemia effects, through its anti‐inflammatory, antisteatotic, and antioxidant properties. [ABSTRACT FROM AUTHOR]