Lipoic acid and Calligonum comosumon attenuate aroclor 1260‐induced testicular toxicity in adult rats

Abstract

Aroclor 1260 is one of the more representative polychlorinated biphenyls found in biota. This study was designed to delineate the testicular toxicity of Aroclor 1260 and to elucidate the potential protective role of Calligonum comosum (C. comosum) and lipoic acid in adult rats. Aroclor 1260 was dissolved in corn oil and given to rats by gavage at doses 0, 20, 40, or 60 mg/kg/day for 15 consecutive days (Groups I, II, III, and IV, respectively). Groups V and VI were pretreated with C. comosum (200 mg/kg/day) and lipoic acid (35 mg/kg/day) respectively 24 h before Aroclor 1260 (40 mg/kg/day) treatment for 15 consecutive days. Aroclor 1260 (20, 40 or 60 mg/kg/day) treatment significantly decreased testes weight, sperm count and motility and daily sperm production. Serum testosterone was significantly decreased in response to treatment with 40 and 60 mg/kg/day of Aroclor 1260. LDH-X activity was significantly decreased at the three dose levels. Hydrogen peroxide (H O ) production (in a dose-related manner) and lipid peroxidation were significantly increased in response to Aroclor 1260 (20, 40, or 60 mg/kg/day) treatment. Aroclor 1260 at the three dose levels decreased the activities of the antioxidant enzymes SOD, CAT, GPx, and GR and the non-enzymatic antioxidant GSH level. CAT, GPx and GSH showed a dose-response effect. These abnormalities were effectively attenuated by pretreatment with C. comosum (200 mg/kg/day) or lipoic acid (35 mg/kg/day). Histopathological examination showed a dose-related increase in morphological abnormalities of the testis in response to Aroclor 1260 treatment. In conclusion, Aroclor 1260 induced testicular toxicity at least, in part, by induction of oxidative stress. By reversal of biochemical and morphological changes towards normalcy, the cytoprotective role of C. comosum and lipoic acid is illuminated. In comparison, lipoic acid was more protective than C. comosum extract against testicular toxicity induced by Aroclor 1260. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1147-1157, 2017.

Testicular toxicity of gentamicin in adult rats: Ameliorative effect of lycopene

“…In the absence of testosterone, germ cells are unable to progress and result in failure of spermatogenesis and infertility. 46,47 The decreased serum testosterone in the gentamicin-treated rats may be due to Leydig cell impairment caused by ROS generation. 48 Pretreatment with lycopene could normalize serum testosterone level by reducing ROS generation.…”

The toxic effects of polychlorinated biphenyl (Aroclor 1242) on Tm3 Leydig cells

“…Moreover, several studies showed that PCBs could increase ROS production, especially hydroxyl radical and hydrogen peroxide (Aly, 2013; Aly et al, 2016; Banudevi et al, 2006; Jiang et al, 2016; Murugesan et al, 2005a, 2005b, 2007a, 2007b, 2008; Senthilkumar et al, 2004; Tunali Ayun and Erkan, 2013; Venkataraman et al, 2008). The results of the present study show that at all A1242 concentrations except for 10 −16 M, there is an increase in hydroxyl radical production; at all concentrations there is an increase in hydrogen peroxide production.…”

“…Previous studies have suggested that PCBs inhibit reproductive functions and ability, cause developmental abnormalities (Aly et al, 2016; Cai et al, 2011, 2013, 2015; Kim, 2001; Kovacevic et al, 1995; Sager, 1983; Sager et al, 1987, 1991; Wakui et al, 2007; Yamamoto et al, 2005), and disrupt the endocrine system (Apostoli et al, 2003) by decreasing testosterone synthesis and steroidogenic enzyme activity in Leydig and Sertoli cells (Fiandanese et al, 2016; Murugesan et al, 2005a, 2005b, 2007a, 2008; Priya et al, 2016; Sridhar et al, 2004). A number of in vitro studies of PCBs’ effects on Leydig cells have shown a direct relationship between sperm formation in testes, reproductive success, and reduced testosterone production (Andric et al, 2000a, 2000b; Johansson, 1989; Kovacevic et al, 1995; Murugesan et al, 2007b; Murugesan et al, 2008).…”

Avaliações toxicológicas das alterações genotóxicas e epigenóticas induzidas por Aroclor 1254 em testí­culo, espermatozóides, fí­gado e rim de camundongos

“…Peróxido de hidrogênio e radical hidroxila parecem ser os principais agentes dos efeitos citotóxicos nos espermatozoides. Um dos principais mecanismos de ação dos PCBs é a indução de estresse oxidativo (ALY,H. A. et al, 2017;ALY, H. A.;ABDEL-NAIM, 2009;AYDIN; ERKAN, 2017).…”

“…a apoptose ou necrose(ALY, H. A.; DOMÈNECH, 2009b; CAITOSAMUEL, 2015). O ion cálcio pode ser um efetor fisiológico e patológico da função mitocondrial que modula a geração deROS (BROOKES et al, 2004).A disfunção das mitocôndrias está associada a algumas doenças, tais como câncer, doenças neurodegenerativas e diabetes tipo 2.…”