Calliandra portoricensisameliorates ovarian and uterine oxido-inflammatory responses inN-methyl-N-nitrosourea and benzo[a]pyrene-treated rats

Abstract

Reproductive dysfunction stemming from chemical agents may lead to infertility. We examined the protective effects of Calliandra portoricensis ( CP) extract on benzo[a]pyrene (BaP) and N-methyl- N-nitrosourea (NMU)-induced ovarian and uterine toxicity in rat, treated as follows: control (group 1), NMU + BaP (group 2), groups 3 and 4 received (NMU + BaP), and CP (50 and 100 mg/kg), respectively. Group 5: CP (100 mg/kg) alone, group 6: (NMU + BaP) and vincristine (VIN: 0.5 mg/kg) and group 7: VIN alone. Rats were injected at age 7, 10, and 13 weeks with single doses of NMU and BaP for 10 consecutive weeks. NMU + BaP significantly ( P < 0.05) increased ovarian and uterine weight, and decreased bodyweight, while the organo-somatic index (OSI) of uterus and ovary increased 2.3 and 1.4 folds, respectively. CP co-treatment ameliorated the observed weight changes. Lipid peroxidation increased by 58% in the ovary, accompanied by decreases in ovarian and uterine GST, GPx, catalase activities, and total sulfhydryl level in NMU + BaP-treated rats. Uterine and ovarian myeloperoxidase activities, as well as nitric oxide levels also increased. CP co-treatment ameliorated the observed changes in antioxidant enzymes and inflammatory biomarkers. Furthermore, histopathology revealed fibrotic ovarian stroma, while uterine endometrium was infiltrated with inflamed cells. Immunohistochemistry showed weak expression of FSH, LH, p53, caspase-3, and Bax, whereas progesterone, iNOS, and Bcl-2 were strongly expressed in NMU + BaP-treated rats. CP treatment restored the architecture of these tissues. Conclusively, the root bark fraction of CP decreases oxido-inflammatory damage in ovarian and uterine tissues of NMU- and BaP-treated rats. Impact statement Infertility resulting from reproductive impairment is traumatic in families. Exposure to chemicals may play insidious roles not easily connected to infertility. We examined benzo[a]pyrene (BaP), and N-methyl nitrosourea (NMU)-induced ovarian and uterine toxicity and the role of Calliandra portoricensis in mitigating toxicity. In a bid to illuminate folk medical claims cloaked in mystery, unearthing lost knowledge, advance natural chemopreventive agents, and report new evidence lacking in the literature attributed to CP. Although CP is known to exhibit anticonvulsant, antidiarrheal, antipyretic, antirheumatic, and analgesic effects in humans, its possible roles for mitigating toxicity stemming from inadvertent chemical exposures are reported here. Our findings affirm and further show that CP abates toxic response incumbent on oxidative damage and inflammatory responses associated with NMU and BaP exposure. Development of phytochemical derived from CP may serve as a potential natural therapy against chemical toxicities in individuals inadvertently exposed, and promote human health and reproductive satiety.

Apigeninidin-rich Sorghum bicolor (L. Moench) extracts suppress A549 cells proliferation and ameliorate toxicity of aflatoxin B1-mediated liver and kidney derangement in rats

“…The total proteins of the liver and kidney tissues were estimated following an established protocol 52 to determine the exact concentration of any protein of interest in the tissue. The markers of oxidative and nitrosative stress in the liver and kidney of rats were determined following well-documented protocols: Superoxide dismutase (SOD) activity 53 , 54 ; catalase (CAT) activity 55 , 56 using H 2 O 2 as a substrate; glutathione S-transferase (GST) activity 57 ; glutathione peroxidase (GPx) activity 58 , 59 ; reduced glutathione (GSH) level 60 , 61 . Also, total sulfhydryl (TSH) level 62 , 63 ; xanthine oxidase (XO) activity 63 , 64 ; myeloperoxidase (MPO) activity 18 , 65 ; nitric oxide (NO) level 48 , 66 were also evaluated accordingly.…”

Caffeic acid mitigates aflatoxinB1‐mediated toxicity in the male rat reproductive system by modulating inflammatory and apoptotic responses, testicular function, and the redox‐regulatory systems

“…Portion of the previously prepared supernatant from the right testis and epididymis was used for the evaluation of oxidative stress in the testis and epididymis. SOD activity was measured by the previously reported method of Misra and Fridovich (1972), Adefisan et al (2020); CAT activity according to the method of Clairborne (1995), Owumi, Nwozo, Effiong, et al (2020). As previously reported, total sulfhydryl group and reduced GSH was assessed by Ellman’s (1959), Arowoogun et al (2020) and Jollow et al (1974), Owumi et al (2019) method respectively.…”

Chlorogenic acid co‐administration abates tamoxifen‐mediated reproductive toxicities in male rats: An experimental approach

“…The supernatant was after that used for the oxidative stress assays. SOD activity was determined by the method described by Misra and Fridovich and as previously reported (Adefisan et al., 2020; Misra & Fridovich, 1972); CAT activity was determined using H 2 O 2 as a substrate according to the process of Clairborne and as previously reported (Clairborne, 1995; Owumi, Nwozo, et al, 2020); protein concentration was determined by the method of Lowry et al, and as previously reported (Lowry et al., 1951); total sulfhydryl group was determined by the process of Ellman (Arowoogun et al., 2021; Ellman, 1959); reduced GSH was determined using the method described by Jollow et al, and as previously reported (Jollow et al., 1974; Owumi, Aliyu‐Banjo et al, 2019); GST was assayed (monitored at 340 nm) using Habig’s method (Habig et al., 1974); GPx activity was determined according to the process of Rotruck et al, and as previously reported (Owumi, Danso, et al, 2020; Rotruck et al., 1973); xanthine oxidase was quantified by the method of Bergmeyer et al and reported recently (Buege & Aust, 1978; Owumi, Elebiyo, et al, 2020) and Lipid peroxidation marker was quantified as malondialdehyde (MDA) according to the method described by Ohkawa and as previously reported (Folayan et al., 2020; Ohkawa et al, 1979) and expressed as μmol MDA/mg protein.…”