Christopher O. Ikediobi

Protective effects of N-acetylcysteine against cadmium-induced damage in cultured rat normal liver cells

In this study, the protective effects of N-acetylcysteine (NAC), a precursor of reduced glutathione, were studied by measuring the viability, the levels of antioxidant enzymes, and by analyzing the cell cycle in cadmium (Cd)-treated rat liver cells. The cells were treated with 150 µM CdCl2 alone or co-treated with 150 µM CdCl2 and 5 mM NAC (2 h pre-, simultaneous or 2 h post-treatment) for 24 h. The viability of the cells treated with 150 µM CdCl2 alone decreased to 40.1%, while that of the cells co-treated with 5 mM NAC (pre-, simultaneous and post-treatment) significantly increased to 83.7, 86.2 and 83.7%, respectively in comparison to the control cells (100%). The catalase enzyme level decreased to undetectable level in the cells treated with CdCl2 alone, while it significantly increased in the co-treated cells (pre-, simultaneous and post-treatment) to 40.1, 34.3 and 13.2%, respectively. In the cells treated with CdCl2 alone, the glutathione peroxidase enzyme level decreased to 78.3%, while it increased in the co-treated cells (pre-, simultaneous, and post-treatment) to 84.5, 83.3 and 87.9%, respectively. The glutathione reductase enzyme level decreased to 56.1% in the cells treated with cadmium alone, but significantly increased in the cells co treated with NAC (pre-, simultaneous and post-treatment) to 79.5, 78.5 and 78.2%, respectively. Cd caused cell cycle arrest at the S and G2/M phases. The co-treatment with NAC inhibited cell cycle arrest by shifting the cells to the G1 phase. These results clearly show the protective effects of NAC against Cd-induced damage in rat liver cells.

Selective Anticancer Activity of Pure Licamichauxiioic-B Acid in Cultured Cell Lines

Abstract The cytotoxic activities of crude extract and pure licamichauxiioic-B compound from stem and root parts of Licania michauxii Prance (LMP) plant were evaluated against brine shrimp larvae and cell cultures. Under in vivo. shrimp assay, both crude extract and the purified compound were active with ED50 values of 122.5 and 32.1 µg/ml, respectively. When tested in four human cancer cell lines, namely, CL-187 (colon adenocarcinoma), MCF-7 (hormone-dependent breast carcinoma), MDA-MB-231 (hormone-independent breast carcinoma), and CRL-2547 (pancreatic carcinoma), the pure compound exhibited 1.5- to about 3-times greater cytotoxic activity than the crude extract. In all cancer cell lines, the LD50 values of crude extract ranged from 33.8 ± 0.9 to 88.1 ± 3.6 µg/ml, while with pure compound the values ranged from 21.6 ± 1.2 to 31.8 ± 4.2 µg/ml. In a noncancerous normal mouse adipose areolar (CCL-1 NCTC clone 929) cell line, the pure compound was found to have an LD50 value greater than 100 µg/ml. Comparison of cytotoxic results of cell cultures revealed that the pure licamichauxiioic-B compound was relatively inactive in noncancerous cell line. The selectivity index for the pure licamichauxiioic-B compound is greater than 3.14 in all cancer cell lines tested.

Mitigative action of monoisoamyl-2,3-dimercaptosuccinate (MiADMS) against cadmium-induced damage in cultured rat normal liver cells.

Cadmium is non-essential, carcinogenic and multitarget pollutant in the environment. Monoisoamyl-2,3-dimercaptosuccinate (MiADMS) is an ester of dimercaptosuccinic acid that acts as an antioxidant and chelator. Therefore, the mitigative action of MiADMS on viability, morphology, antioxidative enzymes and cell cycle were studied on rat liver cells treated with cadmium chloride (CdCl2). The cells were treated with 150 μM CdCl2 alone or cotreated with 300 μM MiADMS (concurrently, 2 h or 4 h post-CdCl2 treatment) for 24 h. The viability of cells treated with CdCl2 alone was decreased in comparison to the control cells. Cotreatment with MiADMS resulted in an increase in cell viability in comparison to the CdCl2 alone treated cells. The CdCl2 treatment altered the morphological shape of the cells, while cotreatment with MiADMS restored the shape. Antioxidative enzymes activities were decreased in the cells treated with CdCl2 alone, while MiADMS cotreatment resulted in an increase in enzyme activities. The CdCl2 arrested the cells in S phase of the cell cycle. Cotreatment with MiADMS alleviated cell cycle arrest by shifting to G1 phase. These results clearly show the mitigative action of MiADMS on CdCl2 toxicity and may suggest that MiADMS can be used as an antidote against cadmium.