Key words:Bisphenol A, L-carnitine, Malondialdehyde, Hydronephrosis, GlutathioneThe present study aimed to explore the protective effects of L-carnitine on the oxidative stress induced by Bisphenol A (BPA) in rat kidneys. Forty male adult rats were allocated into four groups (10 rats each); placebo, BPA (50 mg/kg bwt per os), Lcarnitine (500 mg/kg bwt i.p), and the BPA/L-carnitine-treated group. After 70 days, blood and kidneys were collected for measurement of renal function, oxidative/antioxidative status, histopathological analyses, and gene expression of nrf2. BPA significantly increased serum urea and carnitine levels suggesting renal damage evidenced by hydropic degenerative changes and hydronephrosis. The level of malondialdehyde (MDA) in kidney was elevated along with decline in renal total antioxidant capacity (TAC) and reduced glutathione (GSH) concentrations following challenged with BPA. Notably, the expression of nrf2 mRNA transcript in kidney tissues was down-regulated after BPA-induced toxicity. L-carnitine treatment ameliorates the damaged effects of BPA on kidneys as indicated by low levels of serum urea and carnitine, and renal MDA. Further, L-carnitine enhances the antioxidants (TAC, and GSH), with up-regulation of nrf2 expression in kidney tissues. Our results suggest the renoprotective activity of L-carnitine in BPA-induced kidney injuries through induction of antioxidant system and modulation of oxidative stress.

Acrylamide (ACR) is an unsaturated monomer that entered in various elds however, it is a potent neurotoxic. The present study target is to explore the neuroprotective e cacy of allicin and melatonin on ACR-induced neurotoxicity. Thirty-six male adult rats were non-selectively separated into six groups: placebo, allicin (20 mg/kg b.w daily per os), melatonin (10 mg/kg b.w 3 times/week per os), ACR (50 mg/kg b.w daily per os), ACR + allicin and ACR + melatonin with the same doses. The assessment of brain biomarkers, neurotransmitters, antioxidative status, Nrf2 signalling pathway, and histopathological analyses were performed following 21 days. ACR exposure enhanced the brain lipid and DNA oxidative damage as well as a reduction in the GSH levels. The obvious brain oxidative injuries was contributed to distinct brain dysfunction that was assured by alteration of brain neurotransmitters (serotonin, dopamine, acetylcholine, and acetylcholinesterase), and pathological brain lesions. Furthermore, ACR exposure increased hydroxy deoxy guanosine (8-OHdG), tumor necrosis factor (TNF) and amyloid protein (AB-42).Finally, the mRNA transcripts of brain Keap-1, Nrf2, and NF-kB were up regulated after ACR intoxication. Interestingly, allicin and melatonin alleviated the ACR-induced brain damage assessed by normalization of the mentioned analyses. The present study demonstrated the protective role of both allicin and melatonin on ACR-prompted neuropathy by alleviation of redox imbalance and enhancement of neurotransmitters as well as relieving DNA damage and anti-in ammatory effect.

bisphenol A-induced hepatic toxicity via activation of Nrf2 and inhibition of pro-inflammatory cytokine gene expression in rats. Vet. arhiv 90, 57-68, 2020. AbSTrACT Bisphenol, used in many polycarbonate plastics and epoxy resins industries, exerts toxic effects on mammalian organs. The mechanisms underlying bisphenol toxicity are well understood, however the chemoprevention effects of L-carnitine have not yet been recorded. This study aimed to explore the protective mechanism of L-carnitine against BPA-induced hepatotoxicity. Male rats were randomly distributed into 4 groups of 10 rats each: vehicle (5 mL corn oil/kg), bisphenol (50 mg/kg b.w. orally), L-carnitine (500 mg/kg b.w. i/p), and L-carnitine bisphenol pre-treated groups. Bisphenol was dissolved in corn oil and gavaged for 70 consecutive days. Up-regulation of tumor necrosis factor (6.6-fold), and interleukin 6 (3.2-fold) mRNA transcript, along with suppression of nuclear factor erythroid 2-like 2 (0.4-fold), were recorded, following bisphenol administration. Subsequently, bisphenol provoked oxidative stress and attenuated the antioxidative molecules. Finally, hepatic dysfunction was assessed by elevated serum aminotransferases, alkaline phosphatase, lactate dehydrogenase, glutamyl transferase activities and ammonia levels, with the subsequent decline in serum albumin concentration, which confirmed the inflammatory cell infiltration and hydropic degeneration, and the impairment of lipid profile. Interestingly, co-administration of L-carnitine improved liver function and lipid profile, which was explained by the activation of nuclear factor erythroid 2-like 2 (1.5-fold) mRNA transcript, which augmented the antioxidant levels and suppressed oxidative stress, tumor necrosis factor (2.6fold), and interleukin 6 (1.5-fold) gene expression. In conclusion, L-carnitine exerted hepatoprotective activity against bisphenol toxicity via antioxidant and anti-inflammatory effects.

Acrylamide (ACR) is an unsaturated monomer that entered in various fields however, it is a potent neurotoxic. The present study target is to explore the neuroprotective efficacy of allicin and melatonin on ACR-induced neurotoxicity. Thirty-six male adult rats were non-selectively separated into six groups: placebo, allicin (20 mg/kg b.w daily per os), melatonin (10 mg/kg b.w 3 times/week per os), ACR (50 mg/kg b.w daily per os), ACR + allicin and ACR + melatonin with the same doses. The assessment of brain biomarkers, neurotransmitters, antioxidative status, Nrf2 signalling pathway, and histopathological analyses were performed following 21 days. ACR exposure enhanced the brain lipid and DNA oxidative damage as well as a reduction in the GSH levels. The obvious brain oxidative injuries was contributed to distinct brain dysfunction that was assured by alteration of brain neurotransmitters (serotonin, dopamine, acetylcholine, and acetylcholinesterase), and pathological brain lesions. Furthermore, ACR exposure increased hydroxy deoxy guanosine (8-OHdG), tumor necrosis factor (TNF) and amyloid protein (AB-42). Finally, the mRNA transcripts of brain Keap-1, Nrf2, and NF-kB were up regulated after ACR intoxication. Interestingly, allicin and melatonin alleviated the ACR-induced brain damage assessed by normalization of the mentioned analyses. The present study demonstrated the protective role of both allicin and melatonin on ACR-prompted neuropathy by alleviation of redox imbalance and enhancement of neurotransmitters as well as relieving DNA damage and anti-inflammatory effect.