In recent years, the use of the antioxidant in reducing heavy metal toxicities has increased worldwide. Curcumin has been reported to have a strong antioxidant activity. In this study, we investigated the protective effects of curcumin on lead acetate-induced testicular damage in rats. The sample used 40 male rats divided into 5 groups: negative control (rats were given daily with corn oil); positive control (rats were given daily with lead acetate 50 mg/kg BW orally once in a day for 35 days); and the treatment group (rats were given the curcumin 100 mg, 200 mg, and 400 mg/kg BW orally once in a day for 40 days, and on the 5^th day, were given lead acetate 50 mg/kg BW one h after the curcumin administration). After 40 days, levels of malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GPx) in testicular tissue, and sperm count, motility and viability in the epididymis were measured in rats. Testis samples were also collected for histopathological studies. Results showed that lead acetate administration significantly decreased the SOD, GPx, and increased MDA levels. Lead acetate also decreased the sperm count, motility, viability, and altered histopathological testis (testicular damage, necrosis of seminiferous tubules and loss of spermatid) compared to the negative control. However, administration of curcumin significantly improved the histopathological in testis, increased the sperm count, motility, viability, and also significantly increased the SOD, GPx, and decreased MDA in testis of lead acetate-treated rats. From the results of this study we concluded that the curcumin could be a potent natural product provide a promising protective effect against lead acetate induced testicular toxicity in rats.

Methicillin-resistant Staphylococcus aureus (MRSA) is a S. aureus strain resistant to β-lactam antibiotics and is often associated with livestock, known as livestock-associated (LA)-MRSA. Using molecular typing with multi-locus sequence typing, MRSA clones have been classified in pigs, including clonal complex 398. Livestock-associated-methicillin-resistant S. aureus was first discovered in pigs in the Netherlands in 2005. Since then, it has been widely detected in pigs in other countries. Livestock-associated-methicillin-resistant S. aureus can be transmitted from pigs to pigs, pigs to humans (zoonosis), and humans to humans. This transmission is enabled by several risk factors involved in the pig trade, including the use of antibiotics and zinc, the size and type of the herd, and the pig pen management system. Although LA-MRSA has little impact on the pigs' health, it can be transmitted from pig to pig or from pig to human. This is a serious concern as people in direct contact with pigs are highly predisposed to acquiring LA-MRSA infection. The measures to control LA-MRSA spread in pig farms include conducting periodic LA-MRSA screening tests on pigs and avoiding certain antibiotics in pigs. This study aimed to review the emerging LA-MRSA strains in pig farms.

1 The effects of a novel and selective agonist at the endothelin ET_B receptor, IRL 1620 (Suc-[Glu⁹, Ala^11,15] endothelin-1 (8–21)), were examined in the isolated aorta of the rat. 2 IRL 1620 (1–300 nm) changed neither the resting tone nor the cytosolic Ca²⁺ level ([Ca²⁺]_i) of the aorta without endothelium. In the presence of endothelium, however, IRL 1620 increased endothelial [Ca²⁺]_i with little effect on the muscle tone. In the absence of external Ca²⁺, IRL 1620 still induced a transient increase in endothelial [Ca²⁺]_i. 3 Noradrenaline (100 nm) increased both muscle [Ca²⁺]_i and tension. IRL 1620 (1–300 nm) relaxed the muscle with an increase in endothelial [Ca²⁺]_i only in the presence of endothelium. An inhibitor of nitric oxide synthase, 100 μm N^G-monomethyl-l-arginine, inhibited the relaxant effect of IRL 1620 but not the increase in endothelial [Ca²⁺]_i. 4 In resting and noradrenaline-stimulated aorta, the effects of IRL 1620 were inhibited by a selective antagonist of the ET_B receptor, IRL 1038 (0.3–3 μm), although a selective antagonist of the ET_A receptor, BQ-123 (3 μm), was ineffective. Verapamil (10 μm) did not alter the effects of IRL 1620. 5 A muscarinic receptor agonist, carbachol (1 μm), also induced endothelium-dependent relaxation with an increase in endothelial [Ca²⁺]_i. However, the effects of carbachol were not inhibited by the ET_B antagonist, IRL 1038 (3 μm). 6 These results suggest that IRL 1620 is a selective agonist at the ET_B receptor which increases endothelial [Ca²⁺]_i by releasing Ca²⁺ from storage sites and by opening non-L type Ca²⁺ channels, activates nitric oxide synthase, releases nitric oxide, and relaxes vascular smooth muscle.