The growth-inhibitory activity of materials derived from the fruit of Terminalia chebula was evaluated against six intestinal bacteria by means of an impregnated paper disk agar diffusion method. The butanol fraction of T. chebula extract had profound growth-inhibitory activity at a concentration of 5 mg per disk. The biologically active component isolated from the T. chebula fruits was identified with a variety of spectroscopic analyses as ethanedioic acid. The growth responses varied in accordance with the bacterial strain, chemical, and dosage tested. In a test with concentrations of 2 and 1 mg per disk, ethanedioic acid had strong and moderate inhibitory activity against Clostridium perfringens and Escherichia coli, respectively, with no associated adverse effects on the growth of the four tested lactic acid-producing bacteria. Ellagic acid derived from T. chebula fruits exerted a potent inhibitory effect against C. perfringens and E. coli, but little or no inhibition was observed with treatments of behenic acid, P-caryophyllene, eugenol, isoquercitrin, oleic acid, ca-phellandrene, 3-sitosterol, stearic acid, a-terpinene, terpinen-4-ol, terpinolene, or triacontanoic acid. These results may be an indication of at least one of the pharmacological properties of T. chebula fruits.

The results show that repeated oral doses of MWCNTs during pregnancy induces minimal maternal toxicity and no embryo-fetal toxicity at 1,000 mg/kg/day in rats. The no-observed-adverse-effect level of MWCNTs is considered to be 200 mg/kg/day for dams and 1,000 mg/kg/day for embryo-fetal development. In this study, the dosing formulation was not analyzed to determine the degree of reaggregation (or not), nor were blood levels of CNT's measured in the dosed animals to verify or characterize absorption.

This study was conducted to investigate the potential effects of α-chlorohydrin (ACH) on epididymal function and antioxidant system in male rats. The test chemical was administered to male rats by gavage at doses of 0, 3, 10, and 30 mg/kg/day for 7 days. Twenty-four male rats were randomly assigned to four experimental groups, with six rats in each group. Spermatotoxicity was assessed by measurement of reproductive organ weight, testicular sperm head count, epididymal sperm motility and morphology, histopathologic examination, and oxidative damage analysis in rats. At 30 mg/kg/day, an increase in the incidence of clinical signs, epididymis weight, and gross necropsy findings of the epididymis, a decrease in the sperm motility, and an increased incidence of histopathological changes of the epididymis were observed in a dose-dependent manner. At 10 mg/kg/day, an increased incidence of clinical signs and histopathological changes and decreased sperm motility were observed. In the oxidative damage analysis, an increase in the malondialdehyde concentration and a decrease in the glutathione content and glutathione peroxidase and catalase activities in the epididymal tissue were detected at ≥3 mg/kg/day. The results show that graded doses of ACH elicit depletion of the antioxidant defense system and that the spermatotoxicity of ACH may be due to the induction of oxidative stress.

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