Aim of the work: this study aimed at exploring the effects of lead and cadmium on the thyroid function of workers of welding operation are exposed to welding fumes containing various toxic metals. Subjects and Methods: the level of blood lead and cadmium was measured by atomic absorption spectro-photometry. Thyroid stimulating hormone, free thyroxin, free triiodothyronine in serum were estimated by enzyme immunoassay. Results: the workers with higher level of blood lead level (BLL) (30-60) ug/dl showed high thyroidstimulating hormone level (0.50-9)uIU/ml andno changes in free thyroxine and free triiodothyronine. No changes in free thyroxine, free triiodothyronine and Thyroid-stimulating hormone level in relation to increase in cadmium level. Conclusion: we concluded that higher level of blood lead may cause certain damage to thyroid function leading to subclinical hypothyroidism. We concluded no relation between cadmium level and thyroid hormones. The smokers have higher cadmium level (0.59-9.6)ug/L.

Background: As acetaminophen (APAP) toxicity has become more common in many countries, related cases of poisoning, whether deliberate or unintentional, have been identified as a key contributor to acute liver failure. Aime: To discover if omega-369 fatty acids could protect the liver of male mice from the effects of acetamiophen. Methods: Thirty-five albino male mice were allocated to one of five groups at random. Group 1 served as the "negative control" and received a single intraperitoneal injection (10 ml/kg) of normal saline on the eleventh day of the test following ten days of receiving liquid paraffin orally at a dose of 10 ml/kg. The liquid paraffin was given to group 2 "positive control". Group 3 received Omega 369 (50 mg/kg/80 ml). Group 4 received Omega 369 (100 mg/kg/35 ml). Group 5 received N-acetylcysteine (100 mg/kg/10 ml). The mice were given Omega-369, N-acetylcysteine, and liquid paraffin via oral gavage for 10 days. Results: Group 2 had significantly lower levels of glutathione peroxidase (GP-X) and superoxide dismutase (SOD) than group 1, but significantly greater levels of malondialdehyde (MDA). GP-X and SOD levels were significantly higher in mice given the doses of omega-369, and N-acetylcysteine prior to acetaminophen administration, whereas MDA levels were significantly lower in groups 3, 4, and 5 when compared with group 2. Conclusion: Omega-369 fatty acids, when taken orally, exhibit antioxidative effects and may reduce the risk of acetaminophen-induced liver injury.

Background: Acetaminophen (N-acetyl-para-aminophenol, or APAP) poisoning, whether intentional or accidental, is a major general health problem, with its toxicity prevalence significantly increasing in many countries. Currently, acetaminophen is considered one of the main causes of acute liver failure globally. Aim: The aim of this study was to evaluate the possible hepatoprotective effect of Omega-3,6,9 against acetaminophen-induced hepatotoxicity in albino male mice. Methods: Thirty-five albino male mice were randomly divided into five groups: Group 1 (the negative control) received liquid paraffin orally at a dose of 10 ml/kg for ten days, followed by a single intraperitoneal injection (IP) of 10 ml/kg normal saline on the eleventh day of the test. Group 2 (positive control) received liquid paraffin. Group 3 was treated with Omega-3,6,9 (50 mg/kg/80 mL). Group 4 was treated with Omega-3,6,9 (100 mg/kg/35 mL). Group 5 was treated with N-acetylcysteine (100 mg/kg/10 ml). The mice were treated with Omega-3,6,9, N-acetylcysteine, and liquid paraffin once daily by oral gavage for ten days. Result: TNF-α, IL-10, ALT, and AST levels in the positive control group were significantly higher than those in the negative control group. TNF-α, IL-10, ALT, and AST levels in mice given Omega-3,6,9 (50 mg/kg), Omega-3,6,9 (100 mg/kg), and N-acetylcysteine (100 mg/kg) orally prior to acetaminophen injection were significantly decreased compared to those in the positive control group. Conclusion: Oral intake of Omega-3,6,9 may reduce the risk of acetaminophen-induced liver damage.