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. 2018 Feb 13:5:278-287.
doi: 10.1016/j.toxrep.2018.02.003. eCollection 2018.

The consequence of NAC on sodium arsenite-induced uterine oxidative stress

Moumita Dash  1 , Moulima Maity  1 , Arindam Dey  1 , Hasina Perveen  1 , Shamima Khatun  1 , Lipirani Jana  1 , Sandip Chattopadhyay  1
Affiliations

The consequence of NAC on sodium arsenite-induced uterine oxidative stress

Moumita Dash et al. Toxicol Rep. .

Erratum in

Abstract

Arsenic consumption through drinking water is a worldwide major health problem. Management of arsenic intoxication with invasive, painful therapy using metal chelators is usually used as a conventional treatment strategy in human. In this present study, we examined the efficacy of oral administration of N-acetyl l-cysteine (NAC) in limiting arsenic-mediated female reproductive disorders and oxidative stress in female Wistar rats. The treatment was continued for 8 days (2 estrus cycles) on rats with sodium arsenite (10 mg/Kg body weight) orally. We examined the electrozymographic imprint of three different enzymatic antioxidants in uterine tissue. Rats fed with sodium arsenite exhibited a significant lessening in the activities of superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx). Uterine DNA breakage, necrosis, ovarian and uterine tissue damage, disruption in steroidogenesis were also found in arsenic treated rats. Co-administration of NAC at different doses (50 mg/kg body weight, 100 mg/kg body weight, respectively) significantly reversed the action of uterine oxidative stress markers like malondialdehyde (MDA), conjugated dienes (CD) and non protein soluble thiol (NPSH); and noticeably improved antioxidant status of the arsenic fed rats. This ultimately resulted in the uterine tissue repairing followed by improvement of ovarian steroidogenesis. However, this effective function of NAC might be crucial for the restoration of arsenic-induced female reproductive organ damage in rats.

Keywords: Arsenic; N-acetyl-l-cysteine; Oxidative stress; Uterus.

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Figures

None
Graphical abstract
Fig. 1
Fig. 1
(A–C) catalase, SOD and glutathione peroxidase activity in uterine tissue on native gel. Lane distribution Lane 1: Control; Lane 2: Arsenic; Lane 3: Arsenic + NAC 50; Lane 4: Arsenic + NAC 100. The tissue extracts from rats (co-treated with NAC 50 and NAC 100) containing protein in each lane was electrophoresed on 8.0%, 12% and 8.0% native gel followed by substrate specific development of catalase, SOD and glutathione peroxidase bands respectively. The table under each zymogram represents the band density in terms of percentage.
Fig. 2
Fig. 2
Total serum LDH activity illustrated for the extent of cellular damage. Serum protein in each lane was electrophoresed on agarose gel followed by substrate specific development of LDH bands. Lane distribution Lane 1: Control; Lane 2: Arsenic; Lane 3: Arsenic + NAC 50; Lane 4: Arsenic + NAC 100.
Fig. 3
Fig. 3
(A1) various doses of NAC affect on the DNA fragmentation in uterine cells of female rat treated with arsenic. Lane distribution Lane 1: Control; Lane 2: Arsenic; Lane 3: Arsenic + NAC 50; Lane 4: Arsenic + NAC 100. (A2) The band intensity of DNA at its different positions on the agarose gel is evaluated by Image (J) software, expressed in relative/normalized values, and plotted on a graph. Picture shows that arsenic-induced severe DNA damage is prevented by the different doses of NAC exposure. (B) Arrows show Comet formation in uterine horn cells following arsenic ingestion. Arsenic-induced severe DNA breakage which was noticed in single cell apoptotic damage was noticeably prevented by both the doses of NAC. Panel distribution; B1: Control, B2: Arsenic, B3: Arsenic + NAC 50, B4: Arsenic + NAC 100.
Fig. 4
Fig. 4
(A and B) Uterine and ovarian tissue were implanted in paraffin, serially sectioned laterally at 5 μM stained with eosin and hematoxylin (Harris) and observed under a microscope (magnification 340) to study the uterine (A) and ovarian (B) histo-architecture. The arrows show atretic follicles in ovary of arsenic treated rats. Pictures showed the remarkable loss of secretory cells of uterine tissue along with distortion of endometrial layer. The numbers of atretic follicles were increased in the arsenic exposed group. Different doses of NAC co-treatment significantly secured such arsenic-induced uterine and ovarian disorders. Panel distribution; B1: Control, B2: Arsenic, B3: Arsenic + NAC 50, B4: Arsenic + NAC 100.
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