Sodium fluoride-induced testicular toxicity in rats: the possible modulatory effect of quercetin

To Investigate the possible modulatory effects of quercetin [QE] against sodium fluoride [NaF]-mnduced testicular toxicity in rats and to highlight the underlying mechanisms of such protection. Forty adult male rats were classified into four groups; group [I] was served as control. Group [2] was administered NaF [20 mg/kg/day for 30 consecutive days]. Group [3] was received QE [IS mg/kg/day for 30 consecutive days. Group [4] was received QE 24 h prior to NaF administration for 30 consecutive days. Significant decreases in the normal relative testes weight, testicular lactic dehydrogenase [LDH-x] isoenzyme activity, sperms count and motility as well as daily sperm production were observed. The association of NaF-induced testicular toxicity with oxidative stress cascade was also investigated. Significant elevation in testicular level of salondialdehyde [M DA] accompanied with marked reductions in reduced glutathione [GSH] content and superoxide dismutase [SOD] activity were shown. Treatment with QE prior to NaF revealed marked mitigations in the studied functional parameters of the testes. In addition, the lowered activity of SOD and GSI-I content in the testicular tissue were elevated. The high level of MDA lended to be normalized. The data showed the capability of QE to ameliorate NaF-induced testicular toxicity through its antioxidant potential

transplacental carcinogenic promoting activity of chloroacetonitrile the role of L-ornithine and its relation to glutathione content in embryonic tissue

The possible transplacental carcinogenic promoting activity of chloroacetonitrile [CAN, a by-product of drinking water chlorination process] in timed pregnant mice was studied. The activity was investigated through the assessment of the embryonic ornithine-decarboxylase [ODS] activity in relation to the embryonic glutathione [GSH] content after maternal administration of CAN. CAN was administered orally in a single dose of 25, 50, 70, 100 and 150 mg/kg diluted in 0.2 ml corn oil to the pregnant mice [GD 11.5]. All mice were killed 2 hours after treatment and the embryonic tissue was prepared for analysis. Also, a time course study protocol was studied, CAN was given in a single oral dose of 25 or 75 mg/kg to the pregnant mice and they were killed at 2, 6, 12, 24 and 48 hours post-treatment at GD 11.5. Maternal administration of CAN in doses of 25, 50, 75 mg/kg produced a marked increase in ODC activity expressed as pmole 14CO2/mg protein/30 min., associated with a significant reduction in GSH content. However, treatment with CAN either in a dose of 100 or 150 mg/kg showed significant reductions in ODC activity and GSH content. Concerning time-course study protocol, maternal administration of CAN either in 25 or 75 mg/kg produced a significant increase in the embryonic ODC activity accompanied with a remarkable decrease in GSH content measured at 2, 6, 12, 24 and 48 hours post-maternal treatment. The increase in the embryonic carcinogenic marker ODC which was associated with GSH depletion after administration of non-cytotoxic doses of CAN reflected an indication towards the mechanistic pathway of the transplacental carcinogenic promoting potential of CAN