Bioaccumulation of lead in different organs of Ctenopharyngodon Idella (grass fish) and Tor putitora (Mahseer) fish.

Bioaccumulation of toxic heavy metals in the human body can give rise to adverse health effects, the severity of which depends upon their dosage and duration of exposure. In this study, yearlings of two different species of edible fish, i.e., Tor putitora (Mahseer) and Ctenopharyngodon Idella (grass carp), were exposed to different concentrations of lead nitrate in a controlled environment of aquarium for three different lengths of duration (14, 28, and 60 days). The bioaccumulation of lead in different organs, including gills, skin, muscles, liver, intestine, and swim bladder of the fish, was assessed using atomic absorption spectrometry. Generally, the highest lead concentration was observed in the gills and lowest in the muscles for both species at each experimental dosage and duration. In 14-days exposure, the relative pattern of bioaccumulation in different organs was observed as gill > liver > skin > intestine > swim bladder > muscle for both fish species. Similarly, the pattern of bioaccumulation observed in 28-days exposure was as: gill > liver > intestine > skin > swim bladder > muscle in both species. Whereas, pattern in 60-days exposure was observed as gill > liver > intestine > swim bladder > muscle > skin. The data shows that grass carp had stored higher concentrations of lead than Mahseer, which may be attributed to the fact that they are omnivorous. Furthermore, the lowest bioaccumulation was recorded in the muscles until the 56th day of the exposure, after which the concentration steadily increased in the muscles. The observed pattern highlights the importance of exposure's duration to lead; chronic exposure could result in its bioaccumulation at toxic concentrations in the muscles, which is particularly of concern because the fish muscles are heavily consumed as food worldwide.

The protective role of luteolin against the methotrexate-induced hepato-renal toxicity via its antioxidative, anti-inflammatory, and anti-apoptotic effects in rats.

Methotrexate (MTX) is frequently used drug in treatment of cancer and autoimmune diseases. Unfortunately, MTX has many side effects including the hepato-renal toxicity. In this study, we hypothesized that Luteolin (Lut) exhibits protective effect against the MTX-induced hepato-renal toxicity. In order to investigate our hypothesis, the experiment was designed to examine the effect of exposure of male rats to MTX (20 mg/kg, i.p., at day 9) alone or together with Lut (50 mg/kg, oral for 14 days) compared to the control rats (received saline). The findings demonstrated that MTX treatment induced significant increases in the liver and kidney functions markers in serum samples including Aspartate transaminase (AST), Alanine transaminase (ALT), creatinine, urea and uric acid. MTX also mediated an oxidative stress expressed by elevated malondialdehyde (MDA) level and decreased level of reduced glutathione (GSH), antioxidant enzyme activities, and downregulation of the Nrf2 gene expression as an antioxidant trigger. Moreover, the inflammatory markers (NF-κB, TNF-α, and IL-1ß) were significantly elevated upon MTX treatment. In addition, MTX showed an apoptotic response mediated by elevating the pro-apoptotic (Bax) and lowering the anti-apoptotic (Bcl-2) proteins. All of these changes were confirmed by the observed alterations in the histopathological examination of the hepatic and renal tissues. Lut exposure significantly reversed all the MTX-induced changes in the measured parameters suggesting its potential protective role against the MTX-induced toxicity. Finally, our findings concluded the antioxidative, anti-inflammatory and anti-apoptotic effects of Lut as a mechanism of its protective role against the MTX-induced hepato-renal toxicity in rats.

Long-term treatment with finasteride induces apoptosis and pathological changes in female mice.

Androgenetic alopecia is the most common type of alopecia, and it affects humans of both genders. Finasteride is a type II selective 5α-reductase inhibitor that is administered orally to treat androgenetic alopecia and benign prostatic hyperplasia in human males. However, its effect on the vital organs of females is unknown. This study was designed to investigate the effects of finasteride on the vital organs such as liver, kidney, and heart of female mice. To study the prospective effects of finasteride, female mice were orally administered two doses of finasteride (0.5 and 1.5 mg/kg) once daily for 35 days, and serum levels of various biochemical parameters and histopathology of various organs were examined. The results showed that serum levels of alkaline phosphatase were significantly increased by both high- and low-dose finasteride, whereas cholesterol was significantly increased by the high dose only. Creatine kinase was significantly increased by the high and low doses, whereas glucose was significantly decreased by both doses. Histopathological analysis and DNA damage assays showed that finasteride has adverse effects within both the short and the long periods in female mice. In addition, the proapoptotic genes Bax and caspase-3 were significantly increased by high dose finasteride, whereas the antiapoptotic gene Bcl-2 was significantly decreased by the low and high doses. In conclusion, finasteride is not currently approved for therapeutic use in females, and the findings in this study suggest caution in any future consideration of such use.